Filed under: Food and it's Impact on Our Health
ScienceDaily (Nov. 3, 2009) — Decreased physical activity may have little to do with the recent spike in obesity rates among U.S. adolescents, according to researchers at the Johns Hopkins Bloomberg School of Public Health.
Prompted by growing concern that the increase was due to decreased physical activity associated with increased TV viewing time and other sedentary behaviors, researchers examined the patterns and time trends in physical activity and sedentary behaviors among U.S. adolescents based on nationally representative data collected since 1991. The review found signs indicating that the physical activity among adolescents increased while TV viewing decreased in recent years.
The results are featured in the October 30 online issue of Obesity Reviews.
"Although only one third of U.S. adolescents met the recommended levels of physical activity, there is no clear evidence they had become less active over the past decade while the prevalence of obesity continued to rise," said Youfa Wang, MD, PhD, MS, senior author of the study and an associate professor with the Bloomberg School’s Center for Human Nutrition and the Department of International Health. "During the recent decade, U.S. adolescents had greater access to TV, but significantly fewer of them watched TV for three or more hours per day. In addition, daily physical education attendance rates improved along with the use of physical education class in engaging in physical activity. However, there are considerable differences in the patterns by age, sex and ethnicity."
Wang, along with co-authors Shiru Li, MD, MS, former visiting scholar with the Bloomberg School’s Center for Human Nutrition, and Margarita Treuth, PhD, adjunct associate professor with the Bloomberg School’s Center for Human Nutrition and a professor with the University of Maryland East Shore, examined findings from the nationally representative Youth Risk Behavior Surveillance (YRBS) surveys from 1991 to 2007. The survey included U.S. high school students in grades 9 through 12 and provided information about their physical activities including enrollment and participation in physical education in school and sedentary behaviors including screen time.
Based on these surveys, researchers examined the patterns and time trends and compared the observed physical activity patterns with the national goals set in Healthy People 2010, a comprehensive agenda for improving the health of all Americans. They found that minority students were less likely to be physically active and more likely to engage in sedentary behaviors than white students. Girls were less active than boys and decreased physical activity was related to an increase in age.
"The large gaps between the 2007 achievement and the 2010 targets indicate that the goals are unlikely to be achieved by 2010," said Wang. "Our study suggests that more vigorous efforts are needed to help young Americans engage in adequate regular physical activity and reduce sedentary behaviors, which will help promote good health. In addition, these findings may suggest factors other than physical activity, and sedentary behaviors such as unhealthy eating may play a more important role to help explain the recent increase in obesity."
The research was supported in part by research grants from The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and The Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD).
Filed under: Food and it's Impact on Our Health
A call to bring the world together…
Bringing together voices from all religions, all nations, all backgrounds, the Charter for Compassion seeks to remind the world that we all share the Golden Rule.
Karen Armstrong Dalai Lama Desmond Tutu
The principle of compassion lies at the heart of all religious, ethical and spiritual traditions, calling us always to treat all others as we wish to be treated ourselves. Compassion impels us to work tirelessly to alleviate the suffering of our fellow creatures, to dethrone ourselves from the centre of our world and put another there, and to honour the inviolable sanctity of every single human being, treating everybody, without exception, with absolute justice, equity and respect.
It is also necessary in both public and private life to refrain consistently and empathically from inflicting pain. To act or speak violently out of spite, chauvinism, or self-interest, to impoverish, exploit or deny basic rights to anybody, and to incite hatred by denigrating others—even our enemies—is a denial of our common humanity. We acknowledge that we have failed to live compassionately and that some have even increased the sum of human misery in the name of religion.
We therefore call upon all men and women ~ to restore compassion to the centre of morality and religion ~ to return to the ancient principle that any interpretation of scripture that breeds violence, hatred or disdain is illegitimate ~ to ensure that youth are given accurate and respectful information about other traditions, religions and cultures ~ to encourage a positive appreciation of cultural and religious diversity ~ to cultivate an informed empathy with the suffering of all human beings—even those regarded as enemies.
We urgently need to make compassion a clear, luminous and dynamic force in our polarized world. Rooted in a principled determination to transcend selfishness, compassion can break down political, dogmatic, ideological and religious boundaries. Born of our deep interdependence, compassion is essential to human relationships and to a fulfilled humanity. It is the path to enlightenment, and indispensible to the creation of a just economy and a peaceful global community.
Please join this wonderful cause- Let’s All Work Together to Understand Each Other and Live Compassionately.
Agriculture’s sudden rise, however, came with a price. It introduced infectious-disease epidemics, social stratification, intermittent famines, and large-scale war. Jared Diamond, the UCLA professor and writer, has called the adoption of agriculture nothing less than "the worst mistake in human history"—a mistake, he suggests, from which we have never recovered.
(Notice GRAINS are NOT part of the diet!)
The Hadza
They grow no food, raise no livestock, and live without rules or calendars. They are living a hunter-gatherer existence that is little changed from 10,000 years ago. What do they know that we’ve forgotten?
By Michael Finkel at National Geographic
"I’m hungry," says Onwas, squatting by his fire, blinking placidly through the smoke. The men beside him murmur in assent. It’s late at night, deep in the East African bush. Singing, a rhythmic chant, drifts over from the women’s camp. Onwas mentions a tree he spotted during his daytime travels. The men around the fire push closer. It is in a difficult spot, Onwas explains, at the summit of a steep hill that rises from the grassy plain. But the tree, he adds, spreading his arms wide like branches, is heavy with baboons. There are more murmurs. Embers rise to a sky infinite with stars. And then it is agreed. Everyone stands and grabs his hunting bow.
Onwas is an old man, perhaps over 60—years are not a unit of time he uses—but thin and fit in the Hadza way. He’s maybe five feet tall. Across his arms and chest are the hieroglyphs of a lifetime in the bush: scars from hunts, scars from snakebites, scars from arrows and knives and scorpions and thorns. Scars from falling out of a baobab tree. Scars from a leopard attack. Half his teeth remain. He is wearing tire-tread sandals and tattered brown shorts. A hunting knife is strapped to his hip, in a sheath made of dik-dik hide. He’s removed his shirt, as have most of the other men, because he wants to blend into the night.
Onwas looks at me and speaks for a few moments in his native language, Hadzane. To my ear it sounds strangely bipolar—lilting and gentle for a phrase or two, then jarring and percussive, with tongue clicks and glottic pops. It’s a language not closely related to any other that still exists: to use the linguists’ term, an isolate.
I have arrived in the Hadza homeland in northern Tanzania with an interpreter, a Hadza woman named Mariamu. She is Onwas’s niece. She attended school for 11 years and is one of only a handful of people in the world who can speak both English and Hadzane. She interprets Onwas’s words: Do I want to come?
Merely getting this far, to a traditional Hadza encampment, is not an easy task. Years aren’t the only unit of time the Hadza do not keep close track of—they also ignore hours and days and weeks and months. The Hadza language doesn’t have words for numbers past three or four. Making an appointment can be a tricky matter. But I had contacted the owner of a tourist camp not far outside the Hadza territory to see if he could arrange for me to spend time with a remote Hadza group. While on a camping trip in the bush, the owner came across Onwas and asked him, in Swahili, if I might visit. The Hadza tend to be gregarious people, and Onwas readily agreed. He said I’d be the first foreigner ever to live in his camp. He promised to send his son to a particular tree at the edge of the bush to meet me when I was scheduled to arrive, in three weeks.
Sure enough, three weeks later, when my interpreter and I arrived by Land Rover in the bush, there was Onwas’s son Ngaola waiting for us. Apparently, Onwas had noted the stages of the moon, and when he felt enough time had passed, he sent his son to the tree. I asked Ngaola if he’d waited a long time for me. "No," he said. "Only a few days."
At first, it was clear that everyone in camp—about two dozen Hadza, ranging from infants to grandparents—felt uncomfortable with my presence. There was a lot of staring, some nervous laughs. I’d brought along a photo album, and passing it around helped mitigate the awkwardness. Onwas was interested in a picture of my cat. "How does it taste?" he asked. One photo captured everyone’s attention. It was of me participating in a New Year’s Day polar bear swim, leaping into a hole cut in a frozen lake. Hadza hunters can seem fearless; Onwas regularly sneaks up on leopards and races after giraffes. But the idea of winter weather terrified him. He ran around camp with the picture, telling everyone I was a brave man, and this helped greatly with my acceptance. A man who can leap into ice, Onwas must have figured, is certainly a man who’d have no trouble facing a wild baboon. So on the third night of my stay, he asks if I want to join the hunting trip.
I do. I leave my shirt on—my skin does not blend well with the night—and I follow Onwas and ten other hunters and two younger boys out of camp in a single-file line. Walking through Hadza country in the dark is challenging; thorn bushes and spiked acacia trees dominate the terrain, and even during the day there is no way to avoid being jabbed and scratched and punctured. A long trek in the Hadza bush can feel like receiving a gradual full-body tattoo. The Hadza spend a significant portion of their rest time digging thorns out of one another with the tips of their knives.
At night the thorns are all but invisible, and navigation seems impossible. There are no trails and few landmarks. To walk confidently in the bush, in the dark, without a flashlight, requires the sort of familiarity one has with, say, one’s own bedroom. Except this is a thousand-square-mile bedroom, with lions and leopards and hyenas prowling in the shadows.
For Onwas such navigation is no problem. He has lived all his life in the bush. He can start a fire, twirling a stick between his palms, in less than 30 seconds. He can converse with a honeyguide bird, whistling back and forth, and be led directly to a teeming beehive. He knows everything there is to know about the bush and virtually nothing of the land beyond. One time I showed Onwas a map of the world. I spread it open on the dirt and anchored the corners with stones. A crowd gathered. Onwas stared. I pointed out the continent of Africa, then the country of Tanzania, then the region where he lived. I showed him the United States.
I asked him what he knew about America—the name of the president, the capital city. He said he knew nothing. He could not name the leader of his own country. I asked him, as politely as possible, if he knew anything about any country. He paused for a moment, evidently deep in thought, then suddenly shouted, "London!" He couldn’t say precisely what London was. He just knew it was someplace not in the bush.
About a thousand Hadza live in their traditional homeland, a broad plain encompassing shallow, salty Lake Eyasi and sheltered by the ramparts of the Great Rift Valley. Some have moved close to villages and taken jobs as farmhands or tour guides. But approximately one-quarter of all Hadza, including those in Onwas’s camp, remain true hunter-gatherers. They have no crops, no livestock, no permanent shelters. They live just south of the same section of the valley in which some of the oldest fossil evidence of early humans has been found. Genetic testing indicates that they may represent one of the primary roots of the human family tree—perhaps more than 100,000 years old.
What the Hadza appear to offer—and why they are of great interest to anthropologists—is a glimpse of what life may have been like before the birth of agriculture 10,000 years ago. Anthropologists are wary of viewing contemporary hunter-gatherers as "living fossils," says Frank Marlowe, a Florida State University professor of anthropology who has spent the past 15 years studying the Hadza. Time has not stood still for them. But they have maintained their foraging lifestyle in spite of long exposure to surrounding agriculturalist groups, and, says Marlowe, it’s possible that their lives have changed very little over the ages.
For more than 99 percent of the time since the genus Homo arose two million years ago, everyone lived as hunter-gatherers. Then, once plants and animals were domesticated, the discovery sparked a complete reorganization of the globe. Food production marched in lockstep with greater population densities, which allowed farm-based societies to displace or destroy hunter-gatherer groups. Villages were formed, then cities, then nations. And in a relatively brief period, the hunter-gatherer lifestyle was all but extinguished. Today only a handful of scattered peoples—some in the Amazon, a couple in the Arctic, a few in Papua New Guinea, and a tiny number of African groups—maintain a primarily hunter-gatherer existence. Agriculture’s sudden rise, however, came with a price. It introduced infectious-disease epidemics, social stratification, intermittent famines, and large-scale war. Jared Diamond, the UCLA professor and writer, has called the adoption of agriculture nothing less than "the worst mistake in human history"—a mistake, he suggests, from which we have never recovered.
The Hadza do not engage in warfare. They’ve never lived densely enough to be seriously threatened by an infectious outbreak. They have no known history of famine; rather, there is evidence of people from a farming group coming to live with them during a time of crop failure. The Hadza diet remains even today more stable and varied than that of most of the world’s citizens. They enjoy an extraordinary amount of leisure time. Anthropologists have estimated that they "work"—actively pursue food—four to six hours a day. And over all these thousands of years, they’ve left hardly more than a footprint on the land.
Traditional Hadza, like Onwas and his camp mates, live almost entirely free of possessions. The things they own—a cooking pot, a water container, an ax—can be wrapped in a blanket and carried over a shoulder. Hadza women gather berries and baobab fruit and dig edible tubers. Men collect honey and hunt. Nighttime baboon stalking is a group affair, conducted only a handful of times each year; typically, hunting is a solo pursuit. They will eat almost anything they can kill, from birds to wildebeest to zebras to buffalo. They dine on warthog and bush pig and hyrax. They love baboon; Onwas joked to me that a Hadza man cannot marry until he has killed five baboons. The chief exception is snakes. The Hadza hate snakes.
The poison the men smear on their arrowheads, made of the boiled sap of the desert rose, is powerful enough to bring down a giraffe. But it cannot kill a full-grown elephant. If hunters come across a recently dead elephant, they will crawl inside and cut out meat and organs and fat and cook them over a fire. Sometimes, rather than drag a large animal back to camp, the entire camp will move to the carcass.
Hadza camps are loose affiliations of relatives and in-laws and friends. Each camp has a few core members—Onwas’s two sons, Giga and Ngaola, are often with him—but most others come and go as they please. The Hadza recognize no official leaders. Camps are traditionally named after a senior male (hence, Onwas’s camp), but this honor does not confer any particular power. Individual autonomy is the hallmark of the Hadza. No Hadza adult has authority over any other. None has more wealth; or, rather, they all have no wealth. There are few social obligations—no birthdays, no religious holidays, no anniversaries.
People sleep whenever they want. Some stay up much of the night and doze during the heat of the day. Dawn and dusk are the prime hunting times; otherwise, the men often hang out in camp, straightening arrow shafts, whittling bows, making bowstrings out of the ligaments of giraffes or impalas, hammering nails into arrowheads. They trade honey for the nails and for colorful plastic and glass beads that the women fashion into necklaces. If a man receives one as a gift, it’s a good sign he has a female admirer.
There are no wedding ceremonies. A couple that sleeps at the same fire for a while may eventually refer to themselves as married. Most of the Hadza I met, men and women alike, were serial monogamists, changing spouses every few years. Onwas is an exception; he and his wife, Mille, have been with each other all their adult lives, and they have seven living children and several grandchildren. There was a bevy of children in the camp, with the resident grandmother, a tiny, cheerful lady named Nsalu, running a sort of day care while the adults were in the bush. Except for breast-feeding infants, it was hard to determine which kids belonged to which parents.
Gender roles are distinct, but for women there is none of the forced subservience knit into many other cultures. A significant number of Hadza women who marry out of the group soon return, unwilling to accept bullying treatment. Among the Hadza, women are frequently the ones who initiate a breakup—woe to the man who proves himself an incompetent hunter or treats his wife poorly. In Onwas’s camp, some of the loudest, brashest members were women. One in particular, Nduku, appointed herself my language teacher and spent a good percentage of every lesson teasing me mercilessly, often rolling around in laughter as I failed miserably at reproducing the distinct, tongue-tricky clicks.
Onwas knows of about 20 Hadza groups roaming the bush in his area, constantly swapping members, like a giant square dance. Most conflicts are resolved by the feuding parties simply separating into different camps. If a hunter brings home a kill, it is shared by everyone in his camp. This is why the camp size is usually no more than 30 people—that’s the largest number who can share a good-size game animal or two and feel decently sated.
I was there during the six-month dry season, May through October, when the Hadza sleep in the open, wrapped in a thin blanket beside a campfire—two to six people at each hearth, eight or nine fires spread in a wide semicircle fronting a brush-swept common area. The sleep groupings were various: families, single men, young women (with an older woman as minder), couples. During the rainy season, they construct little domed shelters made of interwoven twigs and long grasses: basically, upside-down bird’s nests. To build one takes no more than an hour. They move camp roughly once a month, when the berries run low or the hunting becomes tough or there’s a severe sickness or death.
No one sleeps alone in Onwas’s camp. He assigned his son Ngaola, the one who had waited a few days by the tree, to stay with me, and Ngaola recruited his friend Maduru to join us. The three of us slept in a triangle, head to toe to head around our fire, though when the mosquitoes were fierce, I slept in my tent.
Ngaola is quiet and introspective and a really poor hunter. He’s about 30 years old and still unmarried; bedeviled, perhaps, by the five-baboon rule. It pains him that his older brother, Giga, is probably the most skilled archer in camp. Maduru is a solid outdoorsman, an especially good honey finder, but something of a Hadza misfit. When a natural snakebite remedy was passed around camp, Maduru was left out of the distribution. This upset him greatly, and Onwas had to spend an hour beside him, an arm slung avuncularly over his shoulder, calming him down.
Maduru is the one who assumes responsibility for me during the nighttime baboon quest. As we move through the bush, he snaps off eye-level acacia branches with thorns the size of toothpicks and repeatedly checks to make sure I’m keeping pace. Onwas leads us to the hill where he’d seen the tree full of baboons.
Here we stop. There are hand signals, some clipped chatter. I’m unsure of what is going on—my translator has remained back at camp. The hunt is only for men. But Maduru taps me on the shoulder and motions for me to follow. The other hunters begin fanning out around the base of the hill, and I tail Maduru as he plunges into the brush and starts to climb. The slope seems practically vertical—hands are required to haul yourself up—and the thickets are as dense as Brillo pads. Thorns slice into my hands, my face. A trickle of blood oozes into my eye. We climb. I follow Maduru closely; I do not want to become separated.
Finally, I understand. We are climbing up, from all sides, toward the baboons. We are trying to startle them, to make them run. From the baboons’ perch atop the hill, there is no place to go but down. The Hadza have encircled the hill; therefore, the baboons will be running toward the hunters. Possibly toward Maduru and me.
Have you ever seen a baboon up close? They have teeth designed for ripping flesh. An adult male can weigh more than 80 pounds. And here we are, marching upward, purposely trying to provoke them. The Hadza are armed with bows and arrows. I have a pocketknife.
We move higher. Maduru and I break out of the undergrowth and onto the rocks. I feel as though I’ve emerged from beneath a blanket. There is a sickle of moon, a breeze. We are near the summit—the top is just over a stack of boulders, maybe 20 feet above our head. The baboon tree is up there, barely out of eyesight.
Then I hear it—a crazed screeching sound. The baboons are aware that something is amiss. The sound is piercing, panicked. I do not speak baboon, but it is not difficult to interpret. Go away! Do not come closer! But Maduru clambers farther, up onto a flat rock. I follow. The baboons are surrounded, and they seem to sense it.
Abruptly, there’s a new sound. The crack of branches snapping overhead. The baboons are descending, shrieking. Maduru freezes, drops to one knee, slides an arrow into position, pulls back the bowstring. He is ready. I’m hiding behind him. I hope, I fervently hope, that no baboons run at us. I reach into my pocket, pull out my knife, unfold it. The blade is maybe two inches long. It feels ridiculous, but that is what I do.
The screeching intensifies. And then, directly over us, in stark silhouette against the backdrop of stars, is a baboon. Scrambling. Moving along the rock’s lip. Maduru stands, takes aim, tracking the baboon from left to right, the arrow slotted, the bowstring at maximum stretch. Every muscle in my body tenses. My head pulses with panic. I grip my knife.
The chief reason the Hadza have been able to maintain their lifestyle so long is that their homeland has never been an inviting place. The soil is briny; fresh water is scarce; the bugs can be intolerable. For tens of thousands of years, it seems, no one else wanted to live here. So the Hadza were left alone. Recently, however, escalating population pressures have brought a flood of people into Hadza lands. The fact that the Hadza are such gentle stewards of the land has, in a way, hurt them—the region has generally been viewed by outsiders as empty and unused, a place sorely in need of development. The Hadza, who by nature are not a combative people, have almost always moved away rather than fight. But now there is nowhere to retreat.
There are currently cattle herders in the Hadza bush, and goat herders, and onion farmers, and corn growers, and sport hunters, and game poachers. Water holes are fouled by cow excrement. Vegetation is trampled beneath cattle’s hooves. Brush is cleared to make way for crops; scarce water is used to irrigate them. Game animals have migrated to national parks, where the Hadza can’t follow. Berry groves and trees that attract bees have been destroyed. Over the past century, the Hadza have lost exclusive possession of as much as 90 percent of their homeland.
None of the other ethnic groups living in the area—the Datoga, the Iraqw, the Isanzu, the Sukuma, the Iramba—are hunter-gatherers. They live in mud huts, often surrounded by livestock enclosures. Many of them look down on the Hadza and view them with a mix of pity and disgust: the untouchables of Tanzania. I once watched as a Datoga tribesman prevented several Hadza women from approaching a communal water hole until his cows had finished drinking.
Dirt roads are now carved into the edges of the Hadza bush. A paved road is within a four-day walk. From many high points there is decent cell phone reception. Most Hadza, including Onwas, have learned to speak some Swahili, in order to communicate with other groups. I was asked by a few of the younger Hadza hunters if I could give them a gun, to make it easier to harvest game. Onwas himself, though he’s scarcely ventured beyond the periphery of the bush, senses that profound changes are coming. This does not appear to bother him. Onwas, as he repeatedly told me, doesn’t worry about the future. He doesn’t worry about anything. No Hadza I met, in fact, seemed prone to worry. It was a mind-set that astounded me, for the Hadza, to my way of thinking, have very legitimate worries. Will I eat tomorrow? Will something eat me tomorrow? Yet they live a remarkably present-tense existence.
This may be one reason farming has never appealed to the Hadza—growing crops requires planning; seeds are sown now for plants that won’t be edible for months. Domestic animals must be fed and protected long before they’re ready to butcher. To a Hadza, this makes no sense. Why grow food or rear animals when it’s being done for you, naturally, in the bush? When they want berries, they walk to a berry shrub. When they desire baobab fruit, they visit a baobab tree. Honey waits for them in wild hives. And they keep their meat in the biggest storehouse in the world—their land. All that’s required is a bit of stalking and a well-shot arrow.
There are other people, however, who do ponder the Hadza’s future. Officials in the Tanzanian government, for starters. Tanzania is a future-oriented nation, anxious to merge into the slipstream of the global economy. Baboon-hunting bushmen is not an image many of the country’s leaders wish to project. One minister has referred to the Hadza as backward. Tanzania’s president, Jakaya Kikwete, has said that the Hadza "have to be transformed." The government wants them schooled and housed and set to work at proper jobs.
Even the one Hadza who has become the group’s de facto spokesperson, a man named Richard Baalow, generally agrees with the government’s aims. Baalow, who adopted a non-Hadza first name, was one of the first Hadza to attend school. In the 1960s his family lived in government-built housing—an attempt at settling the Hadza that soon failed. Baalow, 53, speaks excellent English. He wants the Hadza to become politically active, to fight for legal protection of their land, and to seek jobs as hunting guides or park rangers. He encourages Hadza children to attend the regional primary school that provides room and board to Hadza students during the academic year, then escorts them back to the bush when school is out.
The school-age kids I spoke with in Onwas’s group all said they had no interest in sitting in a classroom. If they went to school, many told me, they’d never master the skills needed for survival. They’d be outcasts among their own people. And if they tried their luck in the modern world—what then? The women, perhaps, could become maids; the men, menial laborers. It’s far better, they said, to be free and fed in the bush than destitute and hungry in the city.
More Hadza have moved to the traditionally Hadza area of Mangola, at the edge of the bush, where, in exchange for money, they demonstrate their hunting skills to tourists. These Hadza have proved that their culture is of significant interest to outsiders and a potential source of income. Yet among the Hadza of Mangola there has also been a surge in alcoholism, an outbreak of tuberculosis, and a distressing rise in domestic violence, including at least one report of a Hadza man who beat his wife to death.
Though the youngsters in Onwas’s group show little interest in the outside world, the world is coming to them. After two million years, the age of the hunter-gatherer is over. The Hadza may hold on to their language; they may demonstrate their abilities to tourists. But it’s only a matter of time before there are no more traditional Hadza scrambling in the hills with their bows and arrows, stalking baboons.
Up on the hill Onwas has led us to, clutching my knife, I crouch behind Maduru as the baboon moves along a fin of rock. And then, abruptly, the baboon stops. He swivels his head. He is so close we could reach out to each other and make contact. I stare into his eyes, too frightened to even blink. This lasts maybe a second. Maduru doesn’t shoot, possibly because the animal is too close and could attack us if wounded—it’s often the poison, not the arrow, that kills. An instant later the baboon leaps away into the bushes.
There is silence for a couple of heartbeats. Then I hear frantic yelping and crashing. It’s coming from the far side of the rock, and I can’t tell if it is human or baboon. It’s both. We thrash through bushes, half-tumbling, half-running, until we reach a clearing amid a copse of acacias.
And there it is: the baboon. On his back, mouth open, limbs splayed. Shot by Giga. A nudge with a toe confirms it—dead. Maduru whistles and shouts, and soon the other hunters arrive. Onwas kneels and pulls the arrow out of the baboon’s shoulder and hands it back to Giga. The men stand around the baboon in a circle, examining the kill. There is no ceremony. The Hadza are not big on ritual. There is not much room in their lives, it seems, for mysticism, for spirits, for pondering the unknown. There is no specific belief in an afterlife—every Hadza I spoke with said he had no idea what might happen after he died. There are no Hadza priests or shamans or medicine men. Missionaries have produced few converts. I once asked Onwas to tell me about God, and he said that God was blindingly bright, extremely powerful, and essential for all life. God, he told me, was the sun.
The most important Hadza ritual is the epeme dance, which takes place on moonless nights. Men and women divide into separate groups. The women sing while the men, one at a time, don a feathered headdress and tie bells around their ankles and strut about, stomping their right foot in time with the singing. Supposedly, on epeme nights, ancestors emerge from the bush and join the dancing. One night when I watched the epeme, I spotted a teenage boy, Mataiyo, sneak into the bush with a young woman. Other men fell asleep after their turn dancing. Like almost every aspect of Hadza life, the ceremony was informal, with a strictly individual choice of how deeply to participate.
With the Hadza god not due to rise for several hours, Giga grabs the baboon by a rear paw and drags the animal through the bush back to camp. The baboon is deposited by Onwas’s fire, while Giga sits quietly aside with the other men. It is Hadza custom that the hunter who’s made the kill does not show off. There is a good deal of luck in hunting, and even the best archers will occasionally face a long dry spell. This is why the Hadza share their meat communally.
Onwas’s wife, Mille, is the first to wake. She’s wearing her only set of clothes, a sleeveless T-shirt and a flower-patterned cloth wrapped about her like a toga. She sees the baboon, and with the merest sign of pleasure, a brief nod of her chin, she stokes the fire. It’s time to cook. The rest of camp is soon awake—everyone is hungry—and Ngaola skins the baboon and stakes out the pelt with sharpened twigs. The skin will be dry in a few days and will make a fine sleeping mat. A couple of men butcher the animal, and cuts of meat are distributed. Onwas, as camp elder, is handed the greatest delicacy: the head.
The Hadza cooking style is simple—the meat is placed directly on the fire. No grill, no pan. Hadza mealtime is not an occasion for politeness. Personal space is generally not recognized; no matter how packed it is around a fire, there’s always room for one more, even if you end up on someone’s lap. Once a cut of meat has finished cooking, anyone can grab a bite.
And I mean grab. When the meat is ready, knives are unsheathed and the frenzy begins. There is grasping and slicing and chewing and pulling. The idea is to tug at a hunk of meat with your teeth, then use your knife to slice away your share. Elbowing and shoving is standard behavior. Bones are smashed with rocks and the marrow sucked out. Grease is rubbed on the skin as a sort of moisturizer. No one speaks a word, but the smacking of lips and gnashing of teeth is almost comically loud.
I’m ravenous, so I dive into the scrum and snatch up some meat. Baboon steak, I have to say, isn’t terrible—a touch gamy, but it’s been a few days since I’ve eaten protein, and I can feel my body perking up with every bite. Pure fat, rather than meat, is what the Hadza crave, though most coveted are the baboon’s paw pads. I snag a bit of one and pop it in my mouth, but it’s like trying to swallow a pencil eraser. When I spit the gob of paw pad out, a young boy instantly picks it up and swallows it.
Onwas, with the baboon’s head, is comfortably above the fray. He sits cross-legged at his fire and eats the cheeks, the eyeballs, the neck meat, and the forehead skin, using the soles of his sandals as a cutting board. He gnaws the skull clean to the bone, then plunges it into the fire and calls me and the hunters over for a smoke.
It is impossible to overstate just how much Onwas—and most Hadza—love to smoke. The four possessions every Hadza man owns are a bow, some arrows, a knife, and a pipe, made from a hollowed-out, soft stone. The smoking material, tobacco or cannabis, is acquired from a neighboring group, usually the Datoga, in exchange for honey. Onwas has a small amount of tobacco, which is tied into a ball inside his shirttail. He retrieves it, stuffs it all into his pipe, and then, holding the pipe vertically, plucks an ember from the fire and places it atop his pipe. Pulsing his cheeks in and out like a bellows, he inhales the greatest quantity of smoke he possibly can. He passes the pipe to Giga.
Then the fun begins. Onwas starts to cough, slowly at first, then rapidly, then uncontrollably with tears bursting from his eyes, then with palms pushing against his head, and then, finally, rolling onto his back, spitting and gasping for air. In the meantime, Giga has begun a similar hacking session and has passed the pipe to Maduru, who then passes the pipe to me. Soon, all of us, the whole circle of men, are hacking and crying and rolling on our backs. The smoke session ends when the last man sits up, grinning, and brushes the dirt from his hair.
With the baboon skull still in the fire, Onwas rises to his feet and claps his hands and begins to speak. It’s a giraffe-hunting story—Onwas’s favorite kind. I know this even though Mariamu, my translator, is not next to me. I know because Onwas, like many Hadza, is a story performer. There are no televisions or board games or books in Onwas’s camp. But there is entertainment. The women sing songs. And the men tell campfire stories, the Kabuki of the bush.
Onwas elongates his neck and moves around on all fours when he’s playing the part of the giraffe. He jumps and ducks and pantomimes shooting a bow when he’s illustrating his own role. Arrows whoosh. Beasts roar. Children run to the fire and stand around, listening intently; this is their schooling. The story ends with a dead giraffe—and as a finale, a call and response.
"Am I a man?" asks Onwas, holding out his hands.
"Yes!" shouts the group. "You are a man."
"Am I a man?" asks Onwas again, louder.
"Yes!" shouts the group, their voices also louder. "You are a man!"
Onwas then reaches into the fire and pulls out the skull. He hacks it open, like a coconut, exposing the brains, which have been boiling for a good hour inside the skull. They look like ramen noodles, yellowish white, lightly steaming. He holds the skull out, and the men, including myself, surge forward and stick our fingers inside the skull and scoop up a handful of brains and slurp them down. With this, the night, at last, comes to an end.
The baboon hunt, it seems, was something of an initiation for me. The next day, Nyudu hacks down a thick branch from a mutateko tree, then carefully carves a bow for me, long and gracefully curved. Several other men make me arrows. Onwas presents me with a pipe. Nkulu handles my shooting lessons. I begin to carry my bow and arrows and pipe with me wherever I go (along with my water-purification kit, my sunscreen, my bug spray, and my eyeglass-cleaning cloth).
I am also invited to bathe with the men. We walk to a shallow, muddy hole—more of a large puddle, with lumps of cow manure bobbing about—and remove our clothes. Handfuls of mud are rubbed against the skin as an exfoliant, and we splash ourselves clean. While Hadza have a word for body odor, the men tell me that they prefer their women not to bathe—the longer they go between baths, they say, the more attractive they are. Nduku, my Hadza language teacher, said she sometimes waits months between baths, though she can’t understand why her husband wants her that way. I also discover, by listening to Mille and Onwas, that bickering with one’s spouse is probably a universal human trait. "Isn’t it your turn to fetch water?" "Why are you napping instead of hunting?" "Can you explain why the last animal brought to camp was skinned so poorly?" It occurs to me that these same arguments, in this same valley, have been taking place for thousands of years.
There are things I envy about the Hadza—mostly, how free they appear to be. Free from possessions. Free of most social duties. Free from religious strictures. Free of many family responsibilities. Free from schedules, jobs, bosses, bills, traffic, taxes, laws, news, and money. Free from worry. Free to burp and fart without apology, to grab food and smoke and run shirtless through the thorns.
But I could never live like the Hadza. Their entire life, it appears to me, is one insanely committed camping trip. It’s incredibly risky. Medical help is far away. One bad fall from a tree, one bite from a black mamba snake, one lunge from a lion, and you’re dead. Women give birth in the bush, squatting. About a fifth of all babies die within their first year, and nearly half of all children do not make it to age 15. They have to cope with extreme heat and frequent thirst and swarming tsetse flies and malaria-laced mosquitoes.
The days I spent with the Hadza altered my perception of the world. They instilled in me something I call the "Hadza effect"—they made me feel calmer, more attuned to the moment, more self-sufficient, a little braver, and in less of a constant rush. I don’t care if this sounds maudlin: My time with the Hadza made me happier. It made me wish there was some way to prolong the reign of the hunter-gatherers, though I know it’s almost certainly too late.
It was my body, more than anything, that let me know it was time to leave the bush. I was bitten and bruised and sunburned and stomachachy and exhausted. So, after two weeks, I told everyone in camp I had to go.
There was little reaction. The Hadza are not sentimental like that. They don’t do extended goodbyes. Even when one of their own dies, there is not a lot of fuss. They dig a hole and place the body inside. A generation ago, they didn’t even do that—they simply left a body out on the ground to be eaten by hyenas. There is still no Hadza grave marker. There is no funeral. There’s no service at all, of any sort. This could be a person they had lived with their entire life. Yet they just toss a few dry twigs on top of the grave. And they walk away.
Filed under: Food and it's Impact on Our Health
From Science Daily
Millie; This article say, “Dieters should focus on limiting the amount of fructose they eat instead of cutting out starchy foods such as bread, rice and potatoes, report the researchers, who propose using new dietary guidelines based on fructose to gauge how healthy foods are”.
ARE THEY CRAZY?? This is awful advice! They should cut out fructose INSTEAD of bread, pastas and potatoes. surely they mean IN ADDITION TO.
ScienceDaily (Dec. 14, 2007) — Here’s one tip for how to eat at the holidays: Don’t take your cues from Santa. The sugary cookies and fat-laden fruitcakes the mythical North Pole resident eats are a no-no. But you don’t have to go no-carb to stay fit at the holidays, either, University of Florida researchers say.
In fact, many dieters may actually be cutting out the wrong foods altogether, according to findings from a UF paper published recently in the European Journal of Nutrition. Dieters should focus on limiting the amount of fructose they eat instead of cutting out starchy foods such as bread, rice and potatoes, report the researchers, who propose using new dietary guidelines based on fructose to gauge how healthy foods are.
"There’s a fair amount of evidence that starch-based foods don’t cause weight gain like sugar-based foods and don’t cause the metabolic syndrome like sugar-based foods," said Dr. Richard Johnson, the senior author of the report, which reviewed several recent studies on fructose and obesity. "Potatoes, pasta, rice may be relatively safe compared to table sugar. A fructose index may be a better way to assess the risk of carbohydrates related to obesity."
They are dead wrong here, those foods ARE converted to sugar almost immediately and then to fats. Part of the reason is that Americans LIVE ON CARBS! Start looking in people grocery carts. Over 50% will tell you they do low fat and don’t eat red meat. What’s in thier carts? Bread, cereal, granola, granola bars, nuts, chips, cookies, sodas, energy drinks, baked goods, sports drinks..all mostly carbs. Son they eat low fat, low protein and high carb…and they are overweight, obese even…68% of them.
Many diets — including the low-carb variety — are based on the glycemic index, which measures how foods affect blood glucose levels. Because starches convert to glucose in the body, these diets tend to limit foods such as rice and potatoes.
While table sugar is composed of both glucose and fructose, fructose seems to be the more dangerous part of the equation, UF researchers say. Eating too much fructose causes uric acid levels to spike, which can block the ability of insulin to regulate how body cells use and store sugar and other nutrients for energy, leading to obesity, metabolic syndrome and type 2 diabetes, said Johnson, the division chief of nephrology and the J. Robert Cade professor of nephrology in the UF College of Medicine. UF researchers first detailed the role of uric acid on insulin resistance and obesity in a 2005 study in rats.
"Certainly we don’t think fructose is the only cause of the obesity epidemic," Johnson said. "Too many calories, too much junk food and too much high-fat food are also part of the problem. But we think that fructose may have the unique ability to induce insulin resistance and features of the metabolic syndrome that other foods don’t do so easily."
About 33 percent of adults in the United States are overweight or obese, according to the Centers for Disease Control and Prevention.
Studies at other institutions have shown that following a low-glycemic diet can reduce the risk for diabetes and heart disease, but the effect could occur because these dieters often are unintentionally limiting fructose as well by cutting out table sugar, Johnson said.
"Processed foods have a lot of sugar," Johnson said. "Probably the biggest source (of fructose) is soft drinks."
Johnson also noted that, in relation to obesity, the type of fructose found in foods doesn’t seem to matter. For example, the fructose in an apple is as problematic as the high-fructose corn syrup in soda. The apple is much more nutritious and contains far less sugar, but eating multiple apples in one sitting could send the body over the fructose edge.
In another UF paper, published in October in the American Journal of Clinical Nutrition, Johnson and his collaborators tracked the rise of obesity and diseases such as diabetes with the rise in sugar consumption. The rates of hypertension, diabetes and childhood obesity have risen steadily over the years.
"One of the things we have learned is this whole epidemic brought on by Western diet and culture tracks back to the 1800s," he said. "Nowadays, fructose and high-fructose corn syrup are in everything."
Aside from soft drinks, fructose can be found in pastries, ketchup, fruits, table sugar and jellies and in many processed foods, including the sugar substitute high fructose corn syrup.
UF researchers plan to test a low-fructose diet in patients soon, Johnson said.
I can tell you how a low fructose diet works; beautifully! My clients, and myself, follow a low glycemic, high fat and protein diet. Just as man has for thousands of years. 50% fat (75% of that organic saturated fats, coconut oil, butter, beef broths), 30% protein (eggs, organic free range chickens, grass fed meat) and 20% carbs (green leafy vegetables, onions, mushrooms, peppers,) one serving of fruit a day…and you are at your 2000 calorie a day perfect diet. It gives you all the nutrients you need, in abundance. Perfect weight control, healthy immune system, high steady energy…it rocks!
Kathleen Melanson, an associate professor of nutrition and food sciences at the University of Rhode Island, said establishing a fructose index for foods could "be an appropriate approach," depending on how foods are classified. It makes sense to limit foods prepared with high fructose corn syrup and table sugar, which often contain empty calories, but fruits are an important part of a person’s diet, she added.
It makes sense to limit foods prepared with high fructose corn syrup? LIMIT high fructose corn syrup?? How about not use it at all? How about stop putting it in OUR food??
"One concern I have always had with the glycemic index is the potential to pigeonhole foods as good or bad," she said. This isn’t about judging character of foods, some foods are good, some are bad…but the right foods, in the right proportions…are crucial.
Filed under: Food and it's Impact on Our Health
From Science Daily
ScienceDaily (Nov. 11, 2009) — A diet high in fructose increases the risk of developing high blood pressure (hypertension), according to a paper being presented at the American Society of Nephrology’s 42nd Annual Meeting and Scientific Exposition in San Diego, California. The findings suggest that cutting back on processed foods and beverages that contain high fructose corn syrup (HFCS) may help prevent hypertension.
Over the last 200 years, the rate of fructose intake has directly paralleled the increasing rate of obesity, which has increased sharply in the last 20 years since the introduction of HFCS. Today, Americans consume 30% more fructose than 20 years ago and up to four times more than 100 years ago, when obesity rates were less than 5%. While this increase mirrors the dramatic rise in the prevalence of hypertension, studies have been inconsistent in linking excess fructose in the diet to hypertension.
Diana Jalal, MD (University of Colorado Denver Health Sciences Center), and her colleagues studied the issue in a large representative population of US adults. They examined 4,528 adults 18 years of age or older with no prior history of hypertension. Fructose intake was calculated based on a dietary questionnaire, and foods such as fruit juices, soft drinks, bakery products, and candy were included. Dr. Jalal’s team found that people who ate or drank more than 74 grams per day of fructose (2.5 sugary soft drinks per day) increased their risk of developing hypertension. Specifically, a diet of more than 74 grams per day of fructose led to a 28%, 36%, and 87% higher risk for blood pressure levels of 135/85, 140/90, and 160/100 mmHg, respectively. (A normal blood pressure reading is below 120/80 mmHg.)
"These results indicate that high fructose intake in the form of added sugars is significantly and independently associated with higher blood pressure levels in the US adult population with no previous history of hypertension," the authors concluded. Additional studies are needed to see if low fructose diets can normalize blood pressure and prevent the development of hypertension.
Study co-authors include Richard Johnson, MD, Gerard Smits, PhD, and Michel Chonchol, MD (University of Colorado Denver Health Sciences Center). Dr. Richard Johnson reports a conflict of interest as the author of "The Sugar Fix." The authors report no other financial disclosures.
The study abstract, "Increased Fructose Intake is Independently Associated with Elevated Blood Pressure. Findings from the National Health and Nutrition Examination Survey (2003-2006)," (TH-FC037) was presented as part of a Free Communications Session during the American Society of Nephrology’s 42nd Annual Meeting and Scientific Exposition on Oct. 29 at the San Diego Convention Center in San Diego, CA.
Adapted from materials provided by American Society of Nephrology, via EurekAlert!, a service of AAAS.
Filed under: Food and it's Impact on Our Health
Oh, Happy Day!!!
ScienceDaily (Nov. 12, 2009) — The "chocolate cure" for emotional stress is getting new support from a clinical trial published online in ACS’ Journal of Proteome Research. It found that eating about an ounce and a half of dark chocolate a day for two weeks reduced levels of stress hormones in the bodies of people feeling highly stressed. Everyone’s favorite treat also partially corrected other stress-related biochemical imbalances.
Sunil Kochhar and colleagues note growing scientific evidence that antioxidants and other beneficial substances in dark chocolate may reduce risk factors for heart disease and other physical conditions. Studies also suggest that chocolate may ease emotional stress. Until now, however, there was little evidence from research in humans on exactly how chocolate might have those stress-busting effects.
In the study, scientists identified reductions in stress hormones and other stress-related biochemical changes in volunteers who rated themselves as highly stressed and ate dark chocolate for two weeks. "The study provides strong evidence that a daily consumption of 40 grams [1.4 ounces] during a period of 2 weeks is sufficient to modify the metabolism of healthy human volunteers," the scientists say.
Filed under: Food and it's Impact on Our Health
A few days ago I had a young man ask me about the carb count in the food I was servings to him, but something in the way he said it made me quickly glance up…he looked frightened. Something didn’t compute…he was about 6’ 2”, in perfect physical shape, young, about 24 or so. I asked’ “You have a blood sugar problem”?
He replied, “ I was just released from Mayo this morning, I was taken to the hospital when I passed out, they said I have diabetes. I asked him what they had told him to eat and how to manage it. As he told me the answer I started getting madder and madder. “They told me”, he said, “ To eat the same foods I am eating now but to eat half the amount!” I was incredulous. He said, his face becoming animated, “But I’m sooo hungry”! When asked what he had for breakfast that morning at the hospital, he told me he had had half of an English Muffin with margarine, half a bowl of oatmeal with 2% milk, and a fruit cup!
As I explained to him how excess carbs and the wrong fats, and lack of fats had gotten him to where he was today…it dawned on him..they were creating a patient for life. I told him my experiences when doctors had told me they were not interested in teaching people top get well to the degree that I did, that they didn’t have time and that they would lose out on income.
So I went on with the conversation, explaining about organic meat, grass fed beef, coconut oil…and why…he just grinned, “I can eat, I don’t have to try to be hungry the rest of my life!”
I obtained a flyer from the company Sanofi Aventis, clearly a company who makes pharmaceuticals..although it never mentions that on the flyer, The accompanying flyer was an advertisement for Insulin.
Here’s the Diet they recommended for a diabetic;
Breakfast; white egg omelet with low fat cheese, spinach, onions, a slice of whole wheat toast, 1 teaspoon light margarine spread, 2/3 cup light yogurt, half a grapefruit and coffee with artificial sweetener.
The Nutrition breakdown;
229 calories- woefully inadequate, he should be getting a third of his calories for the day!
30% of his calories were from fat- too low.
23% of calories were from protein- too low.
And 47% of his calories were from CARBOHYDRATES! No wonder they recommend this diet along with the insulin…he’s gonna need it! Plus he has gotten 17% of needed calcium, 7% of needed iron…this isn’t looking good for his health. He took in 41 mg. of Vitamin C, kinda scary. And he took in 438 IU. of Vitamin A..you need 50,000 a DAY! And it is easily gotten through diet alone.
Next; Lunch; 2 slices rye bread, 2 ounces turkey, 2 slices tomato, low fat cheese, light mayonnaise, small apple and a diet beverage! I swear, it really says that!
Lunch was 367 calories- kinda puny..and who eats 2 ounces of meat on a sandwich?
19% was from fat- way too low.
23% was from protein- are you seeing a pattern here…since these too numbers are always too low…guess what that does to the carb percentages? You guessed it!
Carbs were 58% of this persons intake. Eeeekkk! No way to handle diabetes, and a good way to develop more diabetics.
He did get 59 mg of Vitamin C, big whoop. And 2638 IU of Vitamin A, far short still of that 50,000. He took in 14% of needed calcium, and along with the inadequate Vitamin C…no or low absorption of calcium…which he’s not getting enough of anyway.
So lets look at the whole day,. Dinner was 3 OUNCES of broiled salmon with 2 teaspoons canola oil, a whole wheat dinner roll. mixed greens with olive oil, 2/3 cup brown rice and a packet of sugar free chocolate pudding.
This poor man had 1200 calories. I’d starve to death. 29% was from fat, too low for good health and most of high fats were monounsaturated fats, those fats that make cholesterol stick together in the arteries, leads to heart disease, have no nutrition in them, are rancid and unsafe to ever heat at all.
18% of his calories were from protein, too low. And carbs were at 53%. They should be between 15 and 20% for healthy individuals, which is also ideal for diabetics…doesn’t THAT make sense?
But let’s take a look at the nutrition; the vitamins and minerals he got this day;
122 mg of Vitamin C for the whole day! Dismal.
4271 IU of Vitamin A, we need 50,000 to 75,000 from our diet each day.
He took in 54% of needed calcium…(he’ll need Boniva, Lipitor and then Viagra…)
He took in 51% of needed Iron.
And the FDA, the American Heart Association, the Diabetic Association will tell you this is good nutrition.
It’s a joke, and it pisses me off. They lie to sell drugs, keep the doctors offices and hospitals full. It’s time we all got mad and gave feedback about the way you have been duped into thinking that these illnesses “just happen”…they are preventable!
but not with the FDA approved “diet”.
Filed under: Environmental Issues, Food and it's Impact on Our Health, In The Kitchen with Millie- How To's
Many of ya”ll may not have been born by 1969. Those of us who were adults at that time know the extent to which the "new foods" really are imitation foods even though they are not labeled as such.
Crisco- a crappy, dangerous version of lard.
Margarine- A mix of vegetable oils chemically hardened to make it seem like butter..kinda.
Bouillon cubes- nothing like real stocks. Yucky and salty, and they sure don’t have that same mouth feel..mmmm.
Soy- one of the most dangerous foods; highly processed, too many dangers to go into here.
And all the other hellish stuff that man has created and people have actually learned to like..; shake and bake chicken, TV dinners, instant mashed potatoes, Kool-aid, Hawaiian punch…eeeoooowww. I learned to cook at a young age because my mom couldn’t…and I love great food, like at my grandmothers house..it was filling, healthy…at my parents I was always hungry. I whined to get apple juice instead of Kool-aid, honey instead of sugar, butter instead of margarine, Roman Meal bread instead of all the white stuff. Turns out that traditional is best..that’s why it’s a tradition. Pretty basic.
And it turns out that yes, those kitchen arts that are almost lost, stock making, canning, rendering fats, soap making…doing it from scratch is best, healthiest and saves the environment…and us. And my kids have made fun of me for loving to do things from scratch..but I love it all, paper-making, distilling flowers, making my own skin care products, using a clothesline, sewing…just has always made sense to me…and is immensely satisfying.
My next class is on Traditional Arts; Eat a Traditional Diet, How and Why, Stock and Sauce Making, Yogurt making, The Right Fats and how to use them.
I received this comment on my blog;
“Everyone has they’re opinion on what is right or wrong to eat? "God" speaks in the bible about what is clean and unclean to eat of that of which was provided to us. And also, the grains,fruits,etc.. Anything beyond that would be bad for you. So, it’s not what we eat or don’t eat that is detrimental or not to our health, but the man-made additives that are put into making the foods we eat so it will taste better. I do not condone the slaughter industry and the way they produce meat, however, I am not a vegetarian, but I do try to stay more vegan than meat. I’m still learning how to balance what is better, in a long run,for my health, for our bodies are not our own”.
I replied;
While I do appreciate your opinion and input, but it just so happens that humans get very sick on just eating grains and vegetables. That’s science, not religion. I have my own "belief" system when it comes to God, but I study science and nutrition. If God had not provided meat for us to eat, and the knowledge to prepare it, the human race would not have evolved this far. Since we need meat and fats to be healthy, and God has instructed us to eat well and treat out body as a temple…so we can go forth and do his work, it cannot be wrong morally for us to eat meat.
I speak from the perspective of a recovering vegetarian. I followed that way of eating for almost 25 years…because we had no clean meat to eat! I had problems with it, it didn’t give me the right fats, I developed an allergy to EVERY SINGLE PROTEIN SOURCE associated with a vegetarian diet; SOY (after eating it for 15 years it made me start going into anaphylactic shock), DAIRY (I became seriously allergic to all dairy), NUTS (same reaction as to soy, after eating them all my life). I also became highly sensitized to grains. I got well when I stopped eating these very common allergens. Meats, fats and meats broths have enabled me to repair my immune system. I now eat a diet that man has been evolving on for thousands of years; meat, meat stocks, vegetables and fruits. Remember we have only been eating more grains after we stopped living as hunter-gatherers and began living in cities, somewhere around 1000 to 1100 AD>
Even though Kosher meat is killed kindly, it is not organic. Grass-fed gives me meat and fats that are clean; organic, full of life preserving, immune system building Vitamins A,D and E, and the right composition of fats.
I totally agree with the part of your statement about the additives and chemicals doing us harm. It is PART of the picture…but the most crucial nutrients that Americans are deficient in (calcium, Vitamin A and D, saturated fats) are only available in meat and fats from animals that have been raised in the sun!
So hang on to the limited diets that you are eating in the name of “a belief system”, but know that you will develop health problems and deficiencies as you age… Living on mostly carbs (grains and vegetables) will lead to obesity, a breakdown in your immune system, delicate skin that is prone to dryness and skin cancer, depression for lack of the right saturated fats and lack of energy and endurance.
Please read- The Ethics of Eating Meat by Charles Eisenstein
I put a glycemic index up on my site for ya’ll to work off of. Many of the sites on line has a bazillion things to wade through because they list everything..all the breads, cereals, junk foods, sugar, candies…..stuff I don’t eat, and neither should you. So just follow the percentages; get 50% of your calories from fat, 30% from eggs, grass fed meats, and 20% from low glycemic vegetables. Never go above 50 on the glycemic index…or not very often. I always have fruit at breakfast with my fats and proteins, and veggies with lunch and dinner.
Filed under: Food and it's Impact on Our Health
The process by which agave glucose and inulin are converted into “nectar” is similar to the process by which corn starch is converted into HFCS.
The skinny on natural sugar alternatives is that they are a big, fat business opportunity and therefore worth a closer look. You know that our species is genetically programmed to eat sweets until we pretty much explode. Savvy consumers are constantly trying to avoid not only the dizzying amount of sugar and high-fructose corn syrup in our food supply, but also spooky artificial sweeteners, most of which were discovered by accident by people wearing safety goggles and lab coats. This leaves us to appease our sweet tooth with natural sweeteners, a few of which are having a “moment.” But are they—like Ponzi schemes, unnaturally muscular athletes, and Tequila-born love affairs—just too good to be true?
Ina word…YES!
In spite of manufacturers’ claims, agave “nectar” is not made from the sap of the yucca or agave plant but from the starch of the giant pineapple-like, root bulb. The principal constituent of the agave root is starch, similar to the starch in corn or rice, and a complex carbohydrate called inulin, which is made up of chains of fructose molecules. Technically a highly indigestible fiber, inulin, which does not taste sweet, comprises about half of the carbohydrate content of agave. 34
The process by which agave glucose and inulin are converted into “nectar” is similar to the process by which corn starch is converted into HFCS. 35
The agave starch is subject to an enzymatic and chemical process that converts the starch into a fructose-rich syrup—anywhere from 70 percent fructose and higher according to the agave nectar chemical profiles posted on agave nectar websites.
36
(One agave manufacturer claims that his product is made with “natural” enzymes.) That’s right, the refined fructose in agave nectar is much more concentrated than the fructose in HFCS. For comparison, the high fructose corn syrup used in sodas is 55 percent refined fructose. (A natural agave product does exist in Mexico, a molasses type of syrup from concentrated plant nectar, but availability is limited and it is expensive to produce.)
According to Bianchi, agave “nectar” and HFCS “are indeed made the same way, using a highly chemical process with genetically modified enzymes. They are also using caustic acids, clarifiers, filtration chemicals and so forth in the conversion of agave starches.” The result is a high level of highly refined fructose in the remaining syrup, along with some remaining inulin.
In a confidential FDA letter, Dr. Martin Stutsman of the Food and Drug Administration’s Offce of Labeling Enforcement, explains the FDA’s food labeling laws related to agave nectar: “Corn syrup treated with enzymes to enhance the fructose levels is to be labeled ‘High Fructose Corn Syrup.’” According to Mr. Stutsman, agave requires the label “hydrolyzed inulin syrup.”37
Corn Syrup.’” According to Mr. Stutsman, agave requires the label “hydrolyzed inulin syrup.”37 Even though, like corn, agave is a starch and fber food processed with enzymes, it does not require the label “High Fructose Agave Syrup.” Agave “nectar” is a misnomer; at the very least, it should be labeled “agave syrup.”
Agave syrup comes in two colors: clear or light, and amber. What is this difference? Mr. Bianchi explains: “Due to poor quality control in the agave processing plants in Mexico, sometimes the fructose gets burned after being heated above 140 degrees Fahrenheit, thus creating a darker, or amber color.” However, the labels create the impression of an artisan product—like light or amber beer.
THE SAPONIN PROBLEM
Yucca species are known to contain large quantities of saponins. The industry describes saponins in agave syrup as beneficial: “Agave’s rich density of saponins increases hydration as the soapy, surfactant nature of saponins change the wetting angle of water it contacts. This eases and accelerates cellular water uptake, especially when used with a high-quality salt.”38
However, the truth is that the saponins found in many varieties of agave plants are toxic steroid derivatives, capable of disrupting red blood cells and producing diarrhea and vomiting,39 Agave should be avoided during pregnancy or breastfeeding because they might cause or contribute to miscarriage by stimulating blood flow to the uterus.40 At the very least, agave products should carry a warning label indicating that the product may cause a miscarriage.
JUST SAY NO TO AGAVE
Since the FDA makes no effort to enforce food-labeling laws, consumers cannot be certain that what they are eating is what the label says it is. New sweeteners like agave syrup were introduced into the market to make a profit, not to make consumers healthy. Clever marketing has led mane consumers to believe that the high level of fructose in agave syrup makes it a safe and a natural sweetener. Agave syrup labels do not conform to FDA labeling requirements, thus deepening the false illusion of an unprocessed product. As we have demonstrated here, if a sweetener contains manufactured fructose, it is neither safe, nor natural, especially at levels up to 70 percent.
Agave syrup is a manmade sweetener which has been through a complicated chemical refining process of enzymatic digestion that converts the starch and fiber into the unbound, manmade chemical fructose. While high fructose agave syrup won’t spike your blood glucose levels, the fructose in it may cause mineral depletion, liver inflammation, hardening of the arteries, insulin resistance leading to diabetes, high blood pres-sure, cardiovascular disease and obesity.
If you want something sweet, eat a piece of fruit, not a candy bar labeled as a “health food.”
If you want to create something sweet, use sweeteners that are known to be safer. For uncooked dishes, unheated raw honey or dates work well. For cooked dishes or sweet drinks, a good organic maple syrup, or even freshly juiced apple
juice or orange juice can provide delicious and relatively safe sweetness; dehydrated cane sugar juice or maple sugar may be used in moderation in cookies and desserts that contain nutritious ingredients and good fats such as butter, egg yolks and nuts.
However, to be healthy, we cannot eat sugar all day, no matter how natural the form. One should limit total sweetener consumption to less han fve percent of daily calories. For a diet of 2500 calories per day, that’s less than three tablespoons of honey, maple syrup or dehydrated cane sugar juice, or several pieces of fruit. And many people do best by avoiding sweeteners completely.
The lack of standards in the health food world comes as depressing news; but let this news encourage you to consume more pure and unrefined foods and sweetener sources. Good health depends on wise food choices, and wise food choices depend on constant vigilance.
More on the Agave Industry
In the year 2000, with warrants in hand, federal agents from the Office of Criminal Investigations of the Food and Drug Administration (FDA) came banging on the door of North America’s largest agave nectar distributor, Western Commerce Corporation in California. In an extremely rare case of the FDA protecting consumer interests (rather than supporting big business, while shutting down legitimate and health consciousness competition), they discovered that Western Commerce Corporation was adulterating their agave syrup with high fructose corn syrup (to lower the cost even more and increase profit margins). While the federal agents confiscated material in the warehouse, the owners of Western Commerce Corporation were nowhere to be found. Those who ran the company fled the country with millions of dollars in assets to avoid criminal prosecution.
This adulterated agave syrup (refined fructose) was also labeled as certified organic to fool consumers into thinking they were getting a pure product. This shows you how unverified organic labels are used in the USA. Today, high fructose agave syrup is made primarily by two companies: Nekutli, and IIDEA. A third agave marketer, by the name of Volcanic, has a suspicious claim on their website. “If your agave comes from one of the other two companies in Mexico, something has been added.” They are referring to Nekutli and IIDEA. Their claim is based upon an analysis, which they say shows that Volcanic’s agave nectar has a lower level of refined fructose.
When Western Commerce Corporation was shut down, the large retail establishments in the food industry stayed away from agave syrups. They knew better than to risk lawsuits and consumer fraud. “They understood that agave was criminally mislabeled per the U.S. Code of Federal Regulation labeling laws, with an untried sweetener, new to the market, that contained saponins, and was not clearly approved as safe for use,” explains Mr. Bianchi. For many years following this bust, the supermarket and health food store industry avoided using agave.
But recently, some sellers in the agave syrup field, once quiet, have begun sneaking back into the food and beverage chains. And retail food giants like Whole Foods, Wegman’s, Trader Joe’s and Kroger, who should know better, and who should know the food labeling laws and requirements, still have no hesitation in selling the toxic, unapproved and mislabeled refined fructose agave syrup, as well as products containing it.
Source: Russ Bianchi and the Weston Price Foundation
For References click HERE
Filed under: Food and it's Impact on Our Health, In The Kitchen with Millie- How To's
The huge bones are simmering on the stove..I felt like a cave woman in my kitchen last night…browning huge beef shank bones in my Dutch oven, in luscious coconut oil. So tonight it has been sloowly bubbling for 24 hours..I added carrots, onions, celery..all organic, with bay leaves, crushed peppercorns…Celtic salt.
And as I just tasted it for the first time…I realized that I have never tasted a true beef stock before…the mouth feel is nothing like the insipid, salty stuff I have had. The grass fed beef is heavenly to cook with…amazingly nutritious. The gelatin is developing, it’s silky texture is amazingly satisfying.
Another 24 hours to go…the house smells amazing.
I’m making beet salad from beets I grew, then roasted with the beef bones in the oven last night. I added dill and rice vinegar, light salt. Mmmm
While it’s bubbling….I’m making a flourless chocolate cake. Here’s the recipe;
Flourless Chocolate Cake Topped with Raspberries
- 12 oz semisweet chocolate chips
- 1/2 cup butter
- 1/4 cup sugar
- 1/4 cup water
- 1 teaspoon instant coffee granules
- 3 eggs
Preheat the oven to 425 F.
Butter the bottom and sides of a 9 inch pie plate.
Place a 12 inch square sheet of waxed paper in the plate and butter the waxed paper.
In a medium sized saucepan, combine the chocolate chips, 1/2 cup butter, sugar, water, and coffee granules. Heat over medium heat for 2 to 3 minutes, until the chocolate and butter are melted, stirring constantly.
Remove from the heat and stir in the eggs until the mixture is smooth. Pour into the waxed paper-lined pie plate. Bake for 10 minutes; the cake will not be completely set in the middle. Cool, cover loosely, then chill for 6 to 8 hours, or overnight.
When ready to serve, remove the cake from the refrigerator and allow to sit for 10 minutes. Invert the cake onto a large flat serving dish and remove the waxed paper.
Top with raspberries across the whole top, begin in the middle and work out…letting the raspberry tips straight up.
Filed under: Food and it's Impact on Our Health
Close friends of mine began nagging me a few years ago to check out the company that they were getting coconut oil from, Tropical Traditions. They said the thier coconut oil was the best they’d ever had; unprocessed, made by hand, organic… I had only a few years before began researching saturated fats and the role they play in the body, and eating coconut oil…and was pleased with the organic coconut oil I was already eating. Plus, money was tight and I saw no reason to change to a more expensive product…until I went on the site and read about this wonderful product, and began looking into the differences in virgin oils compared to processed oils.
About 3 weeks ago my friends told me they were having an awesome sale, half off on coconut cream, so I ordered some of thier virgin oil. They sent me a book on the company, how the coconut oil was handmade and the health benefits of unprocessed virgin oil.
First of all, the service was wonderful, customer service was excellent, I got my order quickly…the coconut oil and the cream were in glass jars, not plastic. The packaging was all cardboard, no Styrofoam, no plastic.
I love it. I like the taste, the coconut cream is amazing…I made Coconut Fudge Sauce and it is to die for! The cream is coconut concentrate, I use it just like I would heavy cream in a recipe.
The oil I cook with, bake with, use on my hair, my face, my legs after shaving… Coconut cream has always been my favorite oil, mixed with olive oil..to make bar soap or shampoo.
They also carry coconut; shredded, chips, flour (WAY lower on the glycemic index than other flours, a dream to bake with and gluten free!), They carry organic unrefined palm oil, sesame, extra virgin olive oil, soaps, grass fed meat, organic foods.
Here is what info from thier website;
Independent laboratory analysis shows this to be one of the highest quality coconut oils on the market, having the highest levels of antioxidants. This enhanced Virgin Coconut Oil is now in the US market under the Tropical Traditions Gold Label brand. It meets our strictest standards to earn this designation. Today when you buy Tropical Traditions Gold Label Virgin Coconut Oil, you are buying the highest quality coconut oil we have to offer, and it is still made by hand and benefiting families in the rural areas of the Philippines where the coconuts grow.
Is Virgin Coconut Oil the healthiest oil on earth?
Read the research here!
Read what Weston Price has to say about Coconut Oil.
Characteristics of Our Gold Label Virgin Coconut Oil
This Tropical Traditions Gold Label Virgin Coconut Oil is a truly unrefined coconut oil. This coconut oil is made on Mt. Banahaw and surrounding areas from organic coconuts. Coconuts are used fresh (within 24-48 hours of harvest) from small family farms on Mt. Banahaw and other rural places in Quezon Province, the coconut capital of the Philippines. Only the highest quality coconuts are hand-picked from each harvest. The volcanic soil of Mt. Banahaw makes these organic coconuts some of the most nutritionally rich coconuts in the world! Testing done in independent laboratories reveals higher levels of phenolic antioxidants than other coconut oils. The fresh coconut meat is shredded (wet milled), and then cold-pressed using the water from inside the coconuts to make coconut milk. The milk is then allowed to sit for about half a day, while the oil naturally separates from the heavier water. The oil is then filtered from the curds (coconut solids). No chemical or high-heat treatment is used, and this oil contains no trans fatty acids. We do NOT mass produce this oil. It is made by families who are coconut farmers using old-fashioned traditional methods that have been used in the Philippines for hundreds of years. Our coconut trees and family producers are certified organic according to strict USDA standards.
Tropical Traditions also has a Referral Program, so if you place an order with them as a first-time customer, please select “Referred by a friend” and in the box that says “How did you hear of us?” enter my sponsor ID number… 5541380. By telling Tropical Traditions that I referred you, you will receive a complimentary copy of the book Virgin Coconut Oil: How it has changed people’s lives and how it can change yours! by Brian and Marianita Shilhavy with your first order! This book is filled with testimonies and research showing how healthy coconut oil is, and it also includes over 85 recipes showing how one can incorporate coconut into their diet.
I am thrilled to have found this product and recommend it highly.
Filed under: Basics, Food and it's Impact on Our Health, In The Kitchen with Millie- How To's
I have been happily making chicken stock for quite some time now.. About a year and a half ago, while working at Native Sun, I kept bugging the employees in the meat department about finding me a case of grass fed beef shank bones. Months this went on, to no avail. They said they couldn’t get an answer…then they said no.
I could find them on the internet, but I’ll go to extremes to keep from having something shipped to me..for environmental reasons mainly..but also wanting really fresh bones. The local co-ops want 35. to 50. to join.. What to do? I finally sucked up and went to Whole Foods…whom I certainly don’t trust for lots of reasons, preferring to shop local, not chains..
But a friend called and said she had asked them about the bones and they had them…so I got up the next morning and schlepped all the way out there. and was told they didn’t have them. They apologized and gave me the meat managers card, who would be in the next afternoon. So I waited til then and called, spoke to him and made arrangements to drive out the next afternoon to get them..he would hold them for me.
He didn’t…or rather when I got there, again, the next afternoon in 5 o’clock traffic…he wasn’t there. Seems he had been taken to the hospital for diabetes. Why don’t health food stores teach people how to eat? Classes on nutrition? Anyway, I whine, they look all over, can’t find them. They talked to the store manager, who had them cut 4 the meat off of 3 shanks…a 40 minutes wait…but t5hey did it. While hanging out at the meat counter, I noticed that bison was on sale for 3.99 a POUND. Wow… bought three pounds… Finally heaved the bones out to the car, with help…and at a great price.
The burger I had that night was the best bison burger I’ve ever had, very fresh, perfect. Wow.
And this afternoon I came home and browned, then slow roasted all those shanks and they are gently simmering for the next 2 days..mmmmmmmm.
Beef Stock
about 5 pounds beef shank bones
2 Tablespoons coconut oil
3 pounds meaty rib or neck bones
5 or more quarts cold filtered water
1/2 cup vinegar
3 onions, coarsely chopped
3 carrots, coarsely chopped
several sprigs of fresh thyme, tied together
Heat coconut oil to slightly above medium heat, place shanks bones in oil to brown. Brown on all sides, even the ends of marrow. Then place in a roasting pan, covered, and brown at 325 degrees in the oven for 1 hour.
Place the knuckle and marrow bones in a large pot with vinegar and cover with water. Let stand for one hour.
Place roasted bones the water with them knuckles and stuff. Slowly bring up to a soft simmer and simmer, covered for…the longer the better..up to 72 hours.
Pour the fat out of the roasting pan. Deglaze the roasting pan, add liquid to pot., Add additional water, if necessary, to cover the bones; but the liquid should come no higher than within one inch of the rim of the pot, as the volume expands slightly during cooking. Bring to a boil.
A large amount of scum will come to the top, and it is important to remove this with a spoon. After you have skimmed, reduce heat and add the thyme and crushed peppercorns.
Simmer stock for at least 12 and as long as 72 hours. You will now have a pot of rather repulsive-looking brown liquid containing globs of gelatinous and fatty material. It doesn’t even smell particularly good. But don’t despair. After straining you will have a delicious and nourishing clear broth that forms the basis for many other recipes.
After you have made the stock and reduced it as much as you want, place the pot in the refrigerator and let it cool overnight. All the fat will rise to the top. Boil that fat with twice the amount of water as fat, let it solidify again, and THEN store it in the fridge or freezer. This removes a good amount of the meaty taste, and whatever sediment is in the fat will sink to the bottom of the pot. Use it like you would schmaltz or any other solid fat — especially for frying or in pie crusts!
You can do this with bacon grease, too, although I don’t know why you would want to get RID of bacon flavor!! 
The Response-to-Injury Rabbit Never Developed Atherosclerosis — Why Not?
by Chris Masterjohn
From Cholesterol and Health.com
The pop science version of cholesterol goes something like this: when you eat fatty foods, especially foods rich in animal fat, the saturated fat and cholesterol in these foods wind up in your blood and stick to your arteries. Since saturated fats are solid outside your body, they will be solid inside your body too — depsite the 30-degree increase in average temperature. Arteries are much like pipes. When they get caked up with grease, blood flow is impaired, and a heart attack ensues.
None of the prominent scientists who promoted the idea that cholesterol is a critical factor in the development of heart disease ever believed anything remotely resembling this nonsense. From the beginning, they recognized that atherosclerotic plaque accumulates behind the layer of the artery in contact with the blood, called the endothelium, and that the cholesterol and fat within it is engulfed in white blood cells.
The theory these scientists promoted looked something like this: when the cholesterol level in the blood increases, it penetrates the arterial wall and gets stuck; white blood cells circulating in the blood then enter the arterial wall and gobble up the cholesterol; the accumulation of lipid-loaded white blood cells causes local injury, leading to cell death, calcification, and the development of a collagen-laden "fibrous cap" over the atherosclerotic lesion. When the cap ruptures, the blood clots, blocking the artery and causing a heart attack. This is called the lipid hypothesis.
But is this true? Books and web sites devoted to debunking this theory have come out of the woodwork over the last decade; books defending it have followed suit. Consider the following titles to see just how controversial the idea really is:
- The Cholesterol Myths: Exposing the Fallacy That Saturated Fat and Cholesterol Cause Heart Disease by Uffe Ravnskov, MD, PhD (2000).
- The Great Cholesterol Con: Why everything you’ve been told about cholesterol, diet, and heart disease is wrong! by Anthony Colpo (2006).
- The Cholesterol Wars: The Skeptics vs. the Preponderance of the Evidence by Daniel Steinberg, MD, PhD (2007).
- The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It by Malcolm Kendrick, MD (2007).
So is the theory that cholesterol causes heart disease just a myth? Or are the skeptics truly waging a war against the preponderance of the evidence?
The Cholesterol Debate — What Causes Atherosclerosis?
The truth is that each of these authors makes important points. Were there never any good evidence that cholesterol was involved in heart disease, there would be no National Cholesterol Education Program, no statin empire, and Daniel Steinberg could never have written a book plus over 200 scientific papers on the subject. On the other hand, were there never anything seriously wrong with the mainstream dogma on the issue, Ravnskov, Colpo, Kendrick, and many other authors could never have built their careers around pointing out the gaping holes in the theory.
There is no one cause of "heart disease." "Heart disease" is a heterogeneous compliation of diseases of the heart and blood vessels with many different causes. Some of these include disturbances of the rhythm of the heart, calcification of the middle portion of the blood vessels and calcification of the heart valves, and congestive heart failure. The question I address in this article is whether and in what sense cholesterol is involved in atherosclerosis, the development of fatty and calcified plaques in isolated, raised lesions, which can cause heart attacks by rupturing, clotting, and blocking arteries.
In 1933, the famous proponent of the cholesterol-fed rabbit model Nikolai Anitschkov declared that atherosclerosis had been shown to be of an "infiltrative" character rather than a "degenerative" character and was driven by lipids (fatty substances) rather than by inflammation. He did not deny inflammation was involved, but believed that it was secondary to lipid infiltration. Many opponents continue to claim that the root cause driving heart disease has nothing to do with lipids and everything to do with inflammation and that it is degenerative rather than infiltrative in character.
As we will see below, these are all correct! Atherosclerosis is largely driven by the degeneration of lipids which infiltrate the blood vessel and thereby cause inflammation. Inflammation from other sources may accelerate the process or further the degeneration of the atherosclerotic plaques once they are formed, but the initiating factor for fatty plaques appears to be the degeneration of lipids — especially the degeneration of polyunsaturated fatty acids (PUFA).
In order to begin looking at the evidence, we must go back a century in time to the cholesterol-fed rabbit. The cholesterol-fed rabbit model came on the heels of extensive investigations into what would later be termed the "response-to-injury hypothesis."
The Response-to-Injury Rabbit Model
Around the turn of the twentieth century, research into the cause or causes of heart disease was in full throttle. A 1933 compilation edited by E.V. Cowdry entitled Arteriosclerosis: A Survey of the Problem (New York: Macmillan) contained twenty reviews of investigations into the matter, including statistical relationships, the distribution of the disease in wild animals, the distribution in humans according to race and climate, nutritional influences, the physical and chemical nature of the changes that occur in atherosclerotic tissues, and experimental models of the disease.
Nikolai Anitschkov, who developed the cholesterol-fed rabbit model, wrote the 50-page review of experimental animal models.1 Much of this research was published in German, so Anitschkov’s review is an invaluable resource.
According to Anitschkov, early ideas about the origin of arteriosclerosis — a general term for hardening and damage to the arteries, of which atherosclerosis is a specific type — saw the diseases as a response to injury. The injury was primarily seen as either a mechanical or a toxic factor, and was sometimes believed to be injury to the nerves rather than injury to the blood vessels. Researchers carried out a multitude of experiments on rabbits and other animals, including the following:
- Mechanical damage to the blood vessels including ligating, pulling, pinching, and wounding them, and cauterizing them with galvanic wire or silver nitrate.
- Increasing blood pressure by constricting the blood supply through the aorta, damaging the kidneys, or hanging rabbits up by their feet.
- Severing or irritating certain nerves.
- Injecting rabbits with adrenalin.
- Injecting rabbits with a multitude of toxic factors, including digitalin, strophanthin, adonidin, ergotin, theocin, barium chloride, hydrastin, nicotine, caffeine, formalin, ergosterol, and various salts of acids and heavy metals.
- Injection of diphtheria toxin and many other bacteria cultures or bacterial byproducts.
Most of these methods caused substantial damage to the arteries and resulted in a "regenerative thickening" of one or another type. So the response-to-injury concept is quite real.
Atherosclerosis is Just One Type of Arteriosclerosis
None of these methods, however, produced anything resembling human atherosclerosis. While arteriosclerosis refers to hardening and degeneration of the arteries in general, atherosclerosis is a specific type of arteriosclerosis in which a plaque rich in lipid-loaded white blood cells, cholesterol, fatty acids, calcium, various debris — called an atheroma — invades the innermost layer of the blood vessel wall called the intima, just behind the one-cell-thick layer called the endothelium. If you are not familiar with the anatomy of a blood vessel, you can see a diagram of it here.
The research in Anitschkov’s day suggested that, while various types of arteriosclerosis occurred in humans, atherosclerosis was a much more important cause of death. Anitschkov thus concerned his research with what caused atherosclerosis.
The mechanical injuries to blood vessels or nerves produced a local repair process that involved the proliferation of cells, their congregation around the damaged area, and a resultant thickening of the vessel wall. The results were local rather than systemic, however, and never produced a lesion resembling an atheroma.
Injections of adrenalin produced much more interesting changes that were much more relevant to humans. They produced necrosis (death) of cells in the media followed by extensive calcification. A similar process was observed in some of the blood pressure experiments and in many of the experiments involving injections of metallic, bacterial, or other toxins. These changes, however, were fundamentally different from atherosclerosis, which occurs in the intima.
Medial Calcification and the Vitamin K2 Connection
That does not mean this research is irrelevant. Humans experience this type of medial calcification in diabetes, kidney disease, and aging. It appears to assault the media of arteries and the valves of the heart together. It increases arterial stiffness and decreases the artery’s ability to accomodate moderately high levels of blood pressure. One of the most important factors in this type of calcification appears to be vitamin K2.
Vitamin K-dependent proteins protect against cell death, help clear away the debris that cells leave behind when they do die, and protect against the calcification of soft tissues. In the absence of sufficient vitamin K, these proteins are deformed and fail to work properly. It appears that vitamin K2, found in animal fats and fermented foods, is far more important in this respect than vitamin K1, found in green plant foods. I have written extensively on this subject and argued that vitamin K2 is the "activator X" of Weston Price in my article, On the Trail of the Elusive X Factor: Vitamin K2 Revealed.
Despite the research in Anitschkov’s day suggesting that only atherosclerosis had major clinical importance, research in our own day shows that calcification of the media and valves is critically important to, at a minimum, the 324 million people worldwide who will be diabetic come 2025. For the US population born in 2000, the estimated lifetime risk of type 2 diabetes is one in three.2 In type 2 diabetics, medial calcification increases the risk of mortality from heart disease, stroke, and all causes. It also predicts the incidence of heart disease and stroke, including events that do not produce fatalities, and predicts the likelihood that peripheral artery disease will require limb amputation.3
So the response-to-injury hypothesis has a solid basis of evidence for arteriosclerosis of the media, and this is clinically important — but what causes atheroma, that is, the fatty plaque that causes raised lesions in the intima of the blood vessels?
To answer this question, we must look to the cholesterol-fed rabbit.
The Cholesterol-Fed Rabbit Controversy
In 1909, a researcher at the Military Medical Academy in St. Petersburg named Ignatowski produced atherosclerosis in rabbits by feeding them a diet of meat, eggs, and milk. He was pursuing a hypothesis put forward by Nobel Prize-winning microbiologist I. Metchnikov that dietary protein accelerated aging.4
In 1913, Anitschkov and his partner Chalatov were studying at the same academy and were assigned to follow up Ignatowski’s work. They progressively narrowed down the causative factor to cholesterol by feeding different foods and fractions of foods, finally producing the diease by feeding pure cholesterol dissolved in sunflower oil.4
Rabbits fed sunflower oil alone did not develop atherosclerosis. In the cholesterol-fed rabbits, however, lesions developed that exhibited a remarkable similarity to the human disease. They began as fatty streaks in the intima; circulating white blood cells then invaded the intima and engulfed the cholesterol and fat deposited there, eventually growing into large phagocytic cells that Anitschkov called xanthoma cells and we now call foam cells; eventually the developing plaque protruded into the intima in the form of a raised lesion. The lesion possessed a fatty core rich in crystalized and calcified cholesterol deposits and was covered with a fibrous cap.1
The lesions did not appear everywhere equally, but occurred in specific areas. They were most prominent in the aorta and other large arteries, especially in the areas of the artery wall that experience disturbed blood flow such as the points where the arteries branch. While they did not occur in exactly the same places as human atherosclerotic lesions, the pattern was largely similar and the underlying physiological principle dictating the location of the lesions — mainly the type of blood flow experienced by the artery wall — was the same.1
The rabbits developed cholesterol deposits all throughout their bodies, in their eyes and internal organs. Anitschkov produced a more mild form of the disease, however, by feeding the rabbits milk. In these experiments, the rabbits received a much more moderate amount of cholesterol over a much longer period of time and the resulting disease was much more focused in the arteries.1
One curious difference between rabbits and humans is that when rabbits develop atherosclerosis, their plaques never rupture and they never get heart attacks. The main determinant of plaque rupture according to the current scientific literature is the balance between collagen degradation and collagen synthesis.5 Collagen synthesis requires vitamin C. Most animals, including rabbits, make their own vitamin C, but humans do not.
Atherosclerosis itself probably diminishes the quality of life in many different ways by impeding blood flow and blood vessel function, but it clearly does not inexorably lead to heart attacks. The reason why atherosclerosis produces heart attacks in humans and not rabbits or many other animals might be that humans cannot produce their own vitamin C.
Cholesterol in the Blood, Not the Food
Anitschkov argued against calling cholesterol "the cause" of atherosclerosis, but he considered cholesterol the primary causal factor and the necessary causal factor. Mechanical injuries, adrenalin injections, and other methods used to induce various types of arteriosclerosis would accelerate the development of atheroma when they were combined with cholesterol-feeding, but they would never result in human-like atherosclerosis by themselves.
Anitschkov never concluded from his experiments that cholesterol in the diet caused atherosclerosis in humans, however. To the contrary, he wrote the following:
[I]n human atherosclerosis the conditions are different. It is quite certain that such large quantities of cholesterin are not ingested with the ordinary food. In human patients we have probably to deal with a primary disturbance of the cholesterin metabolism, which may lead to atherosclerosis even if the hypercholesterinemia is less pronounced, provided only that it is of long duration and associated with other injurious factors.
Cholesterol skeptics often argue that the rabbit is irrelevant to the human because it is an herbivore. Cholesterol-feeding has failed to produce atherosclerosis in many other species. This is true, but it misses the point. In the species where cholesterol-feeding alone does not produce atherosclerosis, the blood level of cholesterol does not rise as much as in rabbits. But in all of these species when the level of cholesterol in the blood rises high enough, atherosclerosis ensues. For example, feeding dogs cholesterol alone does not produce atherosclerosis because they turn the cholesterol into bile acids; but inhibiting thyroid hormone stops them from making this conversion, and when combined with cholesterol-feeding, it induces atherosclerosis.
As Steinberg points out, raising blood levels of cholesterol has produced atherosclerosis in baboons, cats, chickens, chimpanzees, dogs, goats, guinea pigs, hamsters, monkeys, mice, parrots, pigs, pigeons, rabbits and rats.
The role of blood cholesterol in human heart disease was supported by research showing that people with a disorder that would eventually be called familial hypercholesterolemia had dramatically increased blood levels of cholesterol and, in youth and middle age, dramatically increased relative risks of heart disease and atherosclerosis. But what caused their high cholesterol levels, and did those levels cause the atherosclerosis, and if so, did this phenomenon have any relevance to the rest of us?
And, if cholesterol was somehow the culprit in all of this, was it merely its concentration in the blood that was at play, or was something very different going on?
Lessons From Familial Hypercholesterolemia
Familial hypercholesterolemia (FH) bears a striking resemblance to the cholesterol-fed rabbit model. In mild cases, it produces earlier and more rapidly developing atherosclerosis compared to the general population. In its severe cases, it results in cholesterol deposits all throughout the body, especially in the liver, kidneys, and eyelids.4
In the mid-1970s, Brown and Goldstein discovered that FH resulted from a single genetic defect in the LDL receptor that made the cells unable to absorb LDL from the bloodstream. Steinberg argues that, since cells jealously guard their cholesterol concentrations by adjusting their synthesis of cholesterol as needed, this showed that FH patients differed from the general population in only one single way: the concentration of cholesterol in their blood.4
The finding drew several more parallels between FH and Anitschkov’s cholesterol-fed rabbits. Anitschkov argued that it was not the mere feeding of cholesterol to the rabbits that produced atherosclerosis, but the overwhelming of their capacity to use and dispose of that cholesterol. FH cells could absorb free cholesterol, but not cholesterol from LDL. Anitschkov’s rabbits developed atherosclerosis when they ate cholesterol, but not when they were injected with it — in which case it would not be packaged into lipoproteins such as LDL, which contain many other substances besides cholesterol. Looking backward, it appears that the common thread running through each model was that the level of LDL in the blood exceeded the capacity of the LDL receptors to move that LDL from the blood to the cells.
The LDL receptor highway was blocked, and the LDL traffic was jammed.
Is Steinberg correct, however, that this changes nothing but the concentration of LDL in the blood? Consider what happens in a traffic jam:
- The concentration of cars in the road increases.
- It takes you longer to get home.
When LDL can’t get from the blood into the cells, its concentration in the blood rises, but it also spends a longer amount of time in the blood. Why would that matter? This would become clear just several years later. At the end of the 1970s, the role of oxidative stress in heart disease would finally become clear.
The Role of Oxidized LDL in Heart Disease
Anitschkov believed that his research showed that atherosclerosis was of an infiltrative character rather than a degenerative character. He believed that cholesterol and other substances naturally permeated the endothelium in order to nourish the other layers of the blood vessels, and proceeded from there into the lymph fluid. When the blood level of cholesterol rose sufficiently, he argued, it entered the intima at a faster rate than it could exit and began to accumulate.
Anitschkov was correct that the disease was driven by an infiltration of lipid, and he was correct that the degeneration of the blood vessel wall was secondary to this infiltration. What he failed to realize, and could not have realized at the time, was that the entire process depended on the degeneration of the lipid.
The Discovery of Oxidized LDL
Beginning in 1979, investigators made a series of revolutionary discoveries revealing this degenerative process. When they incubated cells with LDL in the absence of other serum components, the cells underwent severe damage and began to die within 24 hours. Adding serum or HDL prevented the toxicity.4
In 1981, these researchers discovered that culturing endothelial cells with LDL caused dramatic changes to the LDL, making it denser, more electronegative, and giving it a dramatic ability to accumulate in white blood cells called macrophages. Macrophages are phagocytic, meaning they like to gobble up other things, and they are the precursors to the "foam cells" that populate atherosclerotic plaques. The researchers called this LDL "endothelial cell-modified LDL." Soon after, they discovered that the LDL was being "oxidatively modified" and that not only HDL but vitamin E (which HDL is rich in) prevented the effect.4
Oxidized LDL Causes Injury and Inflammation
Since those early findings, thousands of papers have now been published on the role of oxidized LDL in the development of atherosclerosis. Oxidized LDL causes endothelial cells to secrete "adhesion molecules" and "chemoattractants" that allow white blood cells called monocytes to penetrate in between the endothelial cells and stick to them in the subendothelial space where fatty streaks and atherosclerotic plaques develop.6
Oxidized LDL turns on the expression of genes in monocytes which cause them to convert into macrophages and eventually into foam cells, which makes them gobble up more and more oxidized LDL endlessly — but these macrophages use "scavenger receptors" rather than LDL receptors, so they never take up meaningful amounts of non-oxidized LDL; they only take up oxidized LDL, and it is oxidized LDL itself that initates this endless cycle.7
Oxidized LDL initiates the inflammatory process by causing foam cells to secrete molecules that attract T cells and other inflammatory cells.6 Oxidized LDL enhances the process whereby T cells, foam cells, smooth muscle cells and endothelial cells decrease collagen production and increase collagen degradation, which leads to the rupture of the fibrous plaque.5
Endothelial cells produce nitric oxide, a gas that protects LDL from oxidation, increases blood flow, decreases the adhesion of monocytes to the endothelium, and decreases blood clotting. Oxidized LDL impairs the endothelial cell’s ability to produce nitric oxide.8
In short, oxidized LDL contributes to the entire atherosclerotic process from start to finish. Writers who argue that atherosclerosis has nothing to do with lipids but is all about inflammation and response to injury must contend with the fact that oxidized LDL injures endothelial cells and causes inflammation!
Small, Dense (Pattern B) LDL and Oxidation — Which Comes First?
If it is oxidized LDL rather than LDL per se that contributes to atherosclerosis, the question arises of what causes LDL to oxidize. Since polyunsaturated fatty acids (PUFA) in the LDL membrane are the components that are most vulnerable to oxidation, excess PUFA and insufficient antioxidants would seem to be the most obvious culprits. Endothelial cells, however, secrete a number of oxidative enzymes such as myeloperoxidase and lipoxygenase. LDL is always exposed to endothelial cells in the blood, but if it makes its way into the subendothleial space where it can get stuck in a network of sugary proteins called proteoglycans, it would be exposed to them even more directly. Some researchers have therefore put forward the "response-to-retention hypothesis," wherein the LDL oxidizes in response to getting stuck in the subendothelial space.
In 1988, a case-control study showed that people with a preponderance of small, dense LDL were three times more likely to suffer from a heart attack.9 Researchers subsequently showed that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.10 Then the "response-to-retention" crowd jumped in on the game a few years later and showed that small, dense LDL were much more likely get stuck in test tube versions of the proteoglycan network of the subendothelial space.11
If the response-to-retention hypothesis is true, we are back to the infiltration hypothesis where the accumulation of LDL in the subendothelial space is driving the whole process because the accumulation causes the oxidation. This would be a convenient way of circumventing the enormously embarassing fact that the medical establishment has been pushing highly oxidation-prone PUFA oils for fifty years.
The question is, how are these LDL getting small and dense?
Within the response-to-retention paper, the authors stated that "with decreasing size and increasing density the LDL particles have less of the non-polar core covered with a surface monolayer made of phospholipids and cholesterol."
Where did the phospholipid membrane go?
A group working on lipoprotein (a), or Lp(a), published a paper in July of this year showing that virtually all oxidized LDL in the blood circulates attached to Lp(a). Lp(a) is essentially LDL stuck to a protein called apolipoprotein (a) or apo(a). This group showed that when oxidized LDL and apo(a) are incubated together, many of the oxidized phospholipids transfer directly to the apo(a).12 In other words, when the membrane of LDL begins to oxidize, parts of it hop right off the LDL particle. Could that explain why "less of the non-polar core" would be "covered with a surface monolayer" on some LDL particles?
When Steinberg and his coworkers first described the characteristics of "endothelial cell-modified LDL," one of the most conspicuous changes that occurred to the LDL particles was a marked increase in density.13
A 1997 study confirmed that the LDL taken from people with a preponderance of the small, dense type does indeed oxidize quicker in a test tube, but the oxidation status of the LDL was different before they subjected it to oxidation. The predominantly small, dense LDL had a higher ratio of oxidized-to-reduced coenzyme Q10 and a lower CoQ10-to-vitamin E ratio.14 Since CoQ10 is the first line of defense against LDL oxidation, this study strongly suggested that oxidation of the small, dense LDL had already started.
So here we have a chicken-and-egg question. Does small, dense LDL oxidize more rapidly in a test tube because it is small and dense, or because it is already partially oxidized, and its antioxidant defenses are already partially depleted? Is small, dense LDL more vulnerable to oxidation, or does LDL become small and dense when it becomes oxidized?
If LDL becomes small and dense through oxidation, then even if the test tube studies on its "stickiness" are correct and small, dense LDL is more likely to get stuck in the sugary protein network behind the endothelium, it is the oxidation driving the stickiness and not the stickiness driving the oxidation.
So we are back to square one wondering why the medical establishment never announed an emergency measure to put all the research dollars into discovering just how much damage it had done to everyone who followed its recommendations to use high-PUFA vegetable oils in place of saturated animal fats over the last fifty years.
Oxidized LDL and the PUFA Connection
Let us return to the traffic analogy for a moment. Why would an "LDL traffic jam," wherein the "LDL receptor highway" is blocked contribute to atherosclerosis?
The membrane of LDL contains polyunsaturated fatty acids (PUFA), which are highly vulnerable to oxidation. Cells continuously make antioxidant enzymes and other antioxidant compounds to protect their membrane PUFA. If PUFA start to oxidize, the cell ramps up its antioxidant production. When the liver packs cholesterol into a VLDL particle and secretes it into the blood (where it eventually becomes an LDL particle after delivering some of its nutrients to other tissues), it puts some antioxidants into the package. The PUFA have now left the comparative safety of the liver cell and have only a limited supply of antioxidants. When those antioxidants are used up, the PUFA begin to oxidize, and their oxidation products proceed to damage other components of the lipoprotein. When the oxidation becomes severe, the oxidized LDL winds up in a foam cell in an atherosclerotic plaque.
Let’s draw another analogy, this time to a jar of oil. If you use a jar of oil, you open it, exposing the PUFA within it to the oxygen in the air, but quickly put the cap back on and put it back in the fridge. What would happen if you opened the jar and let it sit on the table at room temperature? Over time, the limited amount of antioxidants in the oil would run out and the PUFA would begin to oxidize. The oil would go rancid.
Pumping LDL into the blood but letting it sit there circulating round and round exposed to oxidants rather than taking it into the shelter of the cell is like opening a jar of oil and leaving it on the table.
LDL taken from people who consume more PUFA, whether from vegetable oil or fish oil, oxidizes more easily in a test tube. Alpha-tocopherol, the major form of vitamin E, does not help.15
The specific components of the oxidized LDL particle that interact with the DNA of monocytes to transform them into macrophages and then into foam cells are oxidized derivatives of linoleic acid, a PUFA found in vegetable oils.16
A 2004 study from Brigham and Women’s Hospital and Harvard School of Public Health showed that in postmenopausal women, the more PUFA they ate, and to a much lesser extent the more carbohydrate they ate, the worse their atherosclerosis became over time. The more saturated fat they ate, the less their atherosclerosis progressed; in the highest intake of saturated fat, the atherosclerosis reversed over time.17
I will cover the topic of saturated fat, PUFA, and heart disease in greater detail in another article on the diet-heart hypothesis. Additionally, I have written a Special Report entitled How Essential Are the Essential Fatty Acids? that provides accurate and thoroughly researched information on the true requirement for PUFA, which is negligible for healthy adults. As part of my Special Reports series, I will be publishing a second PUFA Report later this year that will cover the benefits and dangers of consuming PUFA in amounts larger than the minimum requirements.
Shear Stress Explains the Locations of Plaques and the Benefits of Exercise
As in the cholesterol-fed rabbit, human atherosclerosis occurs in discrete plaques at specific locations. In both species, these plaques occur in locations that experience disturbed blood flow, such as the points where the arteries branch.
Anitschkov showed that the endothelium was more permeable to molecules labeled with dye at these points. Experimental vessel injuries that caused inflammatory responses made the endothelium even more permeable, but even in the absence of any treatment, the endothelium was naturally permeable in these areas.1
Sections of the arterial wall in these areas experience a lower level of shear stress than sections in other areas. Shear stress is the type of pressure that is caused by laminar blood flow, or the flow of blood parallel to the blood vessel wall. Shear stress decreases the permeability of the endothelium by stimulating the production of the proteins that form the junctions between the endothelial cells. Under levels of shear stress approximating those that exist at locations where atherosclerosis develops, easily visualizable gold particles the size of LDL particles slip right in between the endothelial cells, whereas the permeability to these particles is very low under levels of shear stress approximating those that exist where plaques do not develop.18
Shear stress also increases nitric oxide production. Nitric oxide increases blood vessel dilation and blood flow, decreases the adhesion of monocytes to the endothelium, decreases blood clotting, and prevents the oxidation of LDL.6
By increasing blood flow, exercise increases shear stress. Since the average shear stress over time seems to be the critical factor, exercise might help prevent atherosclerosis by decreasing the permeability of the endothelium and increasing nitric oxide production in those areas of the blood vessels where the resting level of shear stress is insufficient for protection.
What About Correlations with High Cholesterol?
Much of the cholesterol debate focuses on correlations with cholesterol. How strong are they? How consistent are they? Why do they show up in young people but not in old, in men more than women?
The debate really misses the point, because since the early 1980s the molecular evidence has made very clear that it is oxidized LDL that contributes to atherosclerosis.
Correlations with cholesterol are likely to be confounded by a variety of factors that simultaneously increase cholesterol levels and contribute to heart disease, like stress and inflammation. In fact, inflammation seems to increase cholesterol synthesis essentially as an accidental byproduct of activating the stress response through an enzyme called Rho. Rho slashes nitric oxide production and thus almost certainly makes a contribution to atherosclerosis. For more information on Rho activation, click here.
Researchers have only recently developed methods for testing levels of oxidized LDL. One group has developed an antibody that recognizes oxidized but not non-oxidized phospholipids. They have shown that the proportion of LDL-associated phospholipids that are oxidized is a much more impressive risk factor for heart disease than LDL, and when it is multiplied by the level of LDL, thus indicating the total concentration of oxidized phospholipids, it is even better. Its predictive value is lower in older people, but still strong.19
Why would the association decline with age? If we look at the totality of the evidence about the mechanisms of atherosclerosis, it appears that oxidized LDL is the necessary initiating factor, but that we should expect its prominence as a contributing factor to decrease over time. Atherosclerosis probably does not develop in the absence of oxidized LDL. Once it does develop, however, and once the oxidized LDL stimulates the formation of foam cells, those foam cells recruit T cells that make their own contribution to the inflammatory process. Animal experiments show that independent sources of inflammation cannot initiate atherosclerosis, but they can aggravate it or accelerate it. Vitamin C deficiency, systemic infection, stress, and many other factors likely make contributions alongside oxidized LDL to the weakening and rupture of the fibrous cap that ultimately leads to a heart attack.
Virtually everyone develops substantial atherosclerosis by the time they are old. In people with more oxidized LDL, it occurs faster, and consequently reaches an advanced stage at a younger age. Inflammation will not help rupture a plaque that does not exist, so it will be much less likely to cause a heart attack in a younger person unless that person has high levels of oxidized LDL and consequently advanced atherosclerosis. In an older population wherein most people have advanced plaques, the factors that weaken the plaque will become much more important than the factors that create the plaque.
Studying the issue is complicated by the fact that we are looking at oxidized LDL in the blood. Once LDL gets oxidized enough, presumably it will wind up in arterial plaque. If there are factors that protect circulating LDL from contact with the tissues it could harm, they could confound the association.
Finally, studies looking at cardiovascular incidence or mortality are confounded by the fact that atherosclerosis is only one type of arteriosclerosis, and arteriosclerosis is only one cause of cardiovascular disease. Medial calcification, arrhythmia, congestive heart failure, or other causes of emboli (particles that can cause vessels) may all contribute to cardiovascular events. Oxidized LDL should only, or at least primarily, correlate with those events caused by atherosclerosis.
So is the Lipid Hypothesis Correct?
So is the lipid hypothesis correct? Not in its original form. The weight of the evidence clearly supports a role for the oxidation of LDL and not the concentration of LDL in the blood in the development of atherosclerosis.
The oxidized lipid hypothesis has an enormous amount of evidence supporting it. The cholesterol-fed rabbit model was a model not merely of hypercholesterolemia but of hyper-oxidized-lipoproteinemia. Antioxidants cause major decreases in atherosclerosis in cholesterol-fed or Watanabe familial hypercholesterolemic rabbit models independent of cholesterol levels.4,20
We should not expect antioxidants to be fully capable of preventing the oxidation of LDL by themselves. As I discuss in my PUFA Report, antioxidants can stop oxidized PUFA from damaging other PUFA, but they can never fully repair the oxidized PUFA. The best they can do is convert it to a hydroxy-fatty acid, and it is the hydroxy versions of linoleic acid that have been shown to convert monocytes to foam cells!
Thus, all three of the following critical factors must be addressed:
- Increasing antioxidant status, especially coenzyme Q10, but also alpha- and gamma-tocopherol.
- Reducing PUFA intake.
- Increasing LDL receptor function to minimize the amount of time LDL spends in the bloodstream.
If concentrations of LDL rise in the blood because the LDL is not being utilized — for example, in familial hypercholesterolemia — then the LDL is exposing its vulnerable PUFA to conditions promoting oxidative stress for too long. The solution should not be to diminish cholesterol synthesis, imparing CoQ10 synthesis along with it, but to increase LDL utilization. The appropriate nutritional strategies for increasing LDL utilization desperately need to be researched.
A recent study showed that curcumin, a component of tumeric, increases the expression of the LDL receptor. This study may provide valuable clues. Thyroid hormone is important to the function of the LDL receptor, and many people likely have suboptimal thyroid status.
The irony in all of this is that there is no evidence to suggest that cholesterol is the culprit. In the rabbit, consuming large amounts of cholesterol increases the exposure of LDL membrane-associated PUFA to oxidation because it causes their translocation from the liver to the blood where they are detached from the cellular environment and less protected. In humans, eating cholesterol in the form of several eggs per day probably decreases the vulnerability of LDL to oxidation. See here.
The higher the concentration of free cholesterol within the LDL particle, the less vulnerable it is to oxidation. By contrast, the higher the concentration of cholesterol that is linked to fatty acids, called "esterified cholesterol," the more vulnerable the LDL is to oxidation.9 Esterified cholesterol primarily exists in the core of the particle. Free cholesterol primarily exists in the surface membrane where the initial oxidation takes place, so cholesterol seems to protect the PUFA from oxidation.
So, does cholesterol cause atherosclerosis? No!
But do blood lipids? Yes. Atherosclerosis is a disease in which degenerating lipids infiltrate the blood vessel wall and cause inflammation and degeneration of the local tissue once they arrive there. Solid evidence has amassed in favor of this view for the last 100 years.
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References
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2. Cheng D. Prevalence, predisposition and prevention of type II diabetes. Nutrition & Metabolism. 2005;2:29.
3. Lehto S, Niskanen L, Suhonen M, Ronnemaa T, Laakso M. Medial Artery Calcification. A Neglected Harbinger of Cardiovascular Complications in Non-Insulin-Dependent Diabetes Mellitus. Arteriosis, Thrombosis, and Vascular Biology. 1996;16:978.
4. Steinberg D, The Cholesterol Wars: The Skeptics vs. The Preponderance of the Evidence.2000; San Diego: Academic Press.
5. Libby P. The molecular mechanisms of the thrombotic complications of atherosclerosis. J Intern Med. 2008;263(5):517-27.
6. Libby P. Inflammation and cardiovascular disease mechanisms. Am J Clin Nutr. 2006;83(suppl):456S-60S.
7. Tontonoz P, Nagy L, Alvarez JG, Thomazy VA, Evans RM. PPARgamma promotes monocyte/macrophage differentiation and uptake of oxidized LDL. Cell. 1998;93(2):241-52.
8. Laufs U, Fata VL, Plutzky J, Liao JK. Upregulation of Endotelial Nitric Oxide Synthase by HMG CoA Reductase Inhibitors. Circulation. 1998;97:1129-1135.
9. Austin MA, Breslow JL, Hennekens CH, Buring JE, Willet WC, Krauss RM. Low-density lipoprotein sublass patterns and risk of myocardial infarction. JAMA 1988;260(13):1917-21.
10. Tribble DL, Holl LG, Wood PD, Krauss RM. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis. 1992;93:189-99.
11. Camejo G, Hurt-Camejo E, Wiklund O, Bondjers G. Association of apo B lipoproteins with arterial proteoglycans: Pathological significance and molecular basis. Atherosclerosis 1998;139:205-222.
12. Bergmark C, Dewan A, Orsoni A, Merki E, Miller ER, Shin M-J, et al. A Novel Function of Lipoprotein (a) as a Preferential Carrier of Oxidized Phospholipids in Human Plasma. J Lipid Res. 2008 Jul 3;[Epub ahead of print]
13. Henriksen T, Mahoney EM, Steinberg D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: Recognition by receptors for acetylated low density lipoproteins. Proc Natl Acad Sci USA. 1981;78(10):6499-6503.
14. de Rijke YB, Bredie SJH, Demacker PNM, Vogelaar JM, Hak-Lemmers HLM, Stalenhoef AFH. The Redox Status of Coenzyme Q10 in Total LDL as an Indicator of In Vivo Oxidative Modification. Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:127-133.
15. Nenseter MS, Drevon CA. Dietary polyunsaturates and peroxidation of low density lipoprotein. Curr Opin Lipidol. 1996;7(1):8-13.
16. Nagy L, Tontonoz P, Alvarez JG, Chen H, Evans RM. Oxidized LDL regulates macrophage gene expression through ligand activation of PPARgamma. Cell. 1998;93(2):229-40.
17. Mozaffarian D, Rimm EB, Herrington DM. Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal.
18. Conklin BS, Vito RP, Changyi C. Effect of Low Shear Stress on Permeability and Occludin Expression in Porcine Artery Endothelial Cells. World J Surg. 2007;31:733-43.
19. Tsimikas S, Brilakis ES, Miller ER, McConnell JP, Lennon RJ, Kornman KS, Witztum JL, Berger PB. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N Engl J Med. 2005;353(1):46-57.
20. Wang Z, Zou J, Cao K, Hsieh TC, Huang Y, Wu JM. Dealcoholized red wine containing known amounts of resveratrol suppresses atherosclerosis in hypercholesterolemic rabbits without affecting plasma lipid levels. Int J Mol Med. 2005;16(4):533-40.
Two nutrition experts argue that you can’t take marketing campaigns at face value
By Adam Voiland
With America’s obesity problem among kids reaching crisis proportions, even junk food makers have started to claim they want to steer children toward more healthful choices. In a study released earlier this year, the Centers for Disease Control and Prevention reported that about 32 percent of children were overweight but not obese, 16 percent were obese, and 11 percent were extremely obese. Food giant PepsiCo, for example, points out on its website that "we can play an important role in helping kids lead healthier lives by offering healthy product choices in schools." The company highlights what it considers its healthier products within various food categories through a "Smart Spot" marketing campaign that features green symbols on packaging. PepsiCo’s inclusive criteria—explained here—award spots to foods of dubious nutritional value such as Diet Pepsi, Cap’n Crunch cereal, reduced-fat Doritos, and Cheetos.
But are wellness initiatives like Smart Spot just marketing ploys? Such moves by the food industry may seem to be a step in the right direction, but ultimately makers of popular junk foods have an obligation to stockholders to encourage kids to eat more—not less—of the foods that fuel their profits, says David Ludwig, a pediatrician and the co-author of a commentary published in this week’s Journal of the American Medical Association that raises questions about whether big food companies can be trusted to help combat obesity. Ludwig and article co-author Marion Nestle, a professor of nutrition at New York University, both of whom have long histories of tracking the food industry, spoke with U.S. News and highlighted some things that junk food makers don’t want you to know about their products and how they promote them.
1. Junk food makers spend billions advertising unhealthy foods to kids.
According to the Federal Trade Commission, food makers spend some $1.6 billion annually to reach children through the traditional media as well the Internet, in-store advertising, and sweepstakes. An article published in 2006 in the Journal of Public Health Policy puts the number as high as $10 billion annually. Promotions often use cartoon characters or free giveaways to entice kids into the junk food fold. PepsiCo has pledged that it will advertise only "Smart Spot" products to children under 12.
2. The studies that food producers support tend to minimize health concerns associated with their products.
In fact, according to a review led by Ludwig of hundreds of studies that looked at the health effects of milk, juice, and soda, the likelihood of conclusions favorable to the industry was several times higher among industry-sponsored research than studies that received no industry funding. "If a study is funded by the industry, it may be closer to advertising than science," he says.
3. Junk food makers donate large sums of money to professional nutrition associations.
The American Dietetic Association, for example, accepts money from companies such as Coca-Cola, which get access to decision makers in the food and nutrition marketplace via ADA events and programs, as this release explains. As Nestle notes in her blog and discusses at length in her book Food Politics, the group even distributes nutritional fact sheets that are directly sponsored by specific industry groups. This one, for example, which is sponsored by an industry group that promotes lamb, rather unsurprisingly touts the nutritional benefits of lamb. The ADA’s reasoning: "These collaborations take place with the understanding that ADA does not support any program or message that does not correspond with ADA’s science-based healthful-eating messages and positions," according to the group’s president, dietitian Martin Yadrick. "In fact, we think it’s important for us to be at the same table with food companies because of the positive influence that we can have on them."
4. More processing means more profits, but typically makes the food less healthy.
Minimally processed foods such as fresh fruits and vegetables obviously aren’t where food companies look for profits. The big bucks stem from turning government-subsidized commodity crops—mainly corn, wheat, and soybeans—into fast foods, snack foods, and beverages. High-profit products derived from these commodity crops are generally high in calories and low in nutritional value.
5. Less-processed foods are generally more satiating than their highly processed counterparts.
Fresh apples have an abundance of fiber and nutrients that are lost when they are processed into applesauce. And the added sugar or other sweeteners increase the number of calories without necessarily making the applesauce any more filling. Apple juice, which is even more processed, has had almost all of the fiber and nutrients stripped out. This same stripping out of nutrients, says Ludwig, happens with highly refined white bread compared with stone-ground whole wheat bread.
6. Many supposedly healthy replacement foods are hardly healthier than the foods they replace.
In 2006, for example, major beverage makers agreed to remove sugary sodas from school vending machines. But the industry mounted an intense lobbying effort that persuaded lawmakers to allow sports drinks and vitamin waters that—despite their slightly healthier reputations—still can be packed with sugar and calories.
7. A health claim on the label doesn’t necessarily make a food healthy.
Health claims such as "zero trans fats" or "contains whole wheat" may create the false impression that a product is healthy when it’s not. While the claims may be true, a product is not going to benefit your kid’s health if it’s also loaded with salt and sugar or saturated fat, say, and lacks fiber or other nutrients. "These claims are calorie distracters," adds Nestle. "They make people forget about the calories." Dave DeCecco, a spokesperson for PepsiCo, counters that the intent of a labeling program such as Smart Spot is simply to help consumers pick a healthier choice within a category. "We’re not trying to tell people that a bag of Doritos is healthier than asparagus. But, if you’re buying chips, and you’re busy, and you don’t have a lot of time to read every part of the label, it’s an easy way to make a smarter choice," he says.
8. The food industry funds front groups that fight antiobesity public health initiatives.
Unless you follow politics closely, you wouldn’t necessarily realize that a group with a name like the Center for Consumer Freedom (CCF) has anything to do with the food industry. In fact,Ludwig and Nestle point out, this group lobbies aggressively against obesity-related public health campaigns—such as the one directed at removing junk food from schools—and is funded, according to the Center for Media and Democracy, primarily through donations from big food companies such as Coca-Cola, Cargill, Tyson Foods, and Wendy’s.
9. The food industry works aggressively to discredit its critics.
According to the new JAMA article, the Center for Consumer Freedom boasts that "[our strategy] is to shoot the messenger. We’ve got to attack [activists'] credibility as spokespersons." Here’s the group’s entry on Marion Nestle.
The bottom line, says Nestle, is quite simple: Kids need to eat less, include more fruits and vegetables, and limit the junk food.
What I want to tell you is to NOT buy food out of packages, if it needs are label to list all the ingredients, you don’t want it! Buy unprocessed food; meat, coconut oil, butter, eggs, vegetables…and a tiny amount of fruit. That’s it, leave the cereals, granola bars, chips, sodas, juices on the grocery shelf. Eat enough healthy fat and protein at each meal, the rest should be veggies. And include traditionally made meat stocks for calcium and iron (think soup from scratch).
Filed under: Food and it's Impact on Our Health, In The Kitchen with Millie- How To's
Yep, it’s true…I’m opening a brothel…LOL!
About a month ago I began offering beef and chicken stocks to my clients. They are an essential part of eating a traditional human diet..there is simply no other way to get the calcium you so desperately need. Since the 50’s people have stopped making stocks. All those stupid commercials for drugs like Boniva say, “when diet and exercise are not enough”….
Guess what? Diet and exercise ARE ALWAYS ENOUGH!! Period! No exceptions..
The response has been incredible, I am now making close to 15 quarts of stock each week. I offer them for pick-up each Monday evening…so let me know what you want…go to my webpage for details.. Please order by Thursday of the week before… Optimum Nutrition – Meat Stocks
I also offer raw butter, coconut milk yogurt, salad dressings and fresh mayonnaise, along with gluten free wedding cakes and desserts.
Filed under: Food and it's Impact on Our Health
For the Overweight, Bad Advice by the Spoonful
By GINA KOLATA in the New York Times
Robyn Beck
And I’m making comments in red….
Two-thirds of Americans are overweight or obese. For most, research shows, neither diets nor moderate exercise brings significant long-term weight loss.
At least they get this right, “diets” don’t work…because people diet by cutting caloric intake, which in turn, cuts nutrient intake…and most people do that while lowering fat and protein intake, thinking it is healthier…it’s not….it only leads to eating carbs (fruits and veggies are 95% carbohydrates)…the body goes into starvation mode, not trusting that you are going to keep eating…and no weight loss occurs. Quite the contrary.
In Brief:
Weight control is not simply a matter of willpower. Genes help determine the body’s "set point," which is defended by the brain.
Health and Weight loss are a matter of cause and effect; our bodies react to what we are doing day to day. I was an extremely unhealthy and fat baby…and now am extremely thin and have been since I was 5 years old. I have had clients who weighed over 500 pounds and through proper nutrition took it off easily and have kept it off…and NOT through caloric restriction…but good solid traditional diet. Your bone size is a set point, it’s not going to change (unless you experience bone loss through poor nutrition)…but fat? Completely controllable through getting off empty carbs and eating enough fat6 and protein to get healthy and maintain perfect weight.
Dieting alone is rarely successful, and relapse rates are high. See above.
Moderate exercise, too, rarely results in substantive long-term weight loss, which requires intensive exercise.
And it takes burning 3500 calories to burn off one pound of body fat. I can run 10 miles at a 10 minute a mile clip and only burn about 450 top 500 calories!
Americans have been getting fatter for years, and with the increase in waistlines has come a surplus of conventional wisdom. If we could just return to traditional diets, if we just walk for 20 minutes a day, exercise gurus and government officials maintain, America’s excess pounds would slowly but surely melt away.
If we could just return to traditional diets they say! YES!!! A diet like your grandmother probably cooked…at least mine did, lots of meat, pan dripping and gravies, rich soups, eggs, lots of greens. But we also had lots of breads and sweets. But it wasn’t every day we had sweets, and when we did they were made with butter or lard (NOT Crisco!). In other words, real food.
When I say a traditional diet, I mean what is traditional for humans going back thousands of years; meat, fat, vegetables, fruits, nuts, herbs… Not stuff out of a box, nothing processed.
Scientists are less sanguine. Many of the so-called facts about obesity, they say, amount to speculation or oversimplification of the medical evidence. Diet and exercise do matter, they now know, but these environmental influences alone do not determine an individual’s weight. Body composition also is dictated by DNA and monitored by the brain. Bypassing these physical systems is not just a matter of willpower.
Body composition is fixed..in other words, I’m never going to be stocky, taller, muscular…but my weight I can control….. and so can everyone else. It’s called choices, making the choice to give up the sodas all day, cookies, cereals, sports drinks, ice cream, corn syrup, McDonalds, 750 calorie lattes, energy drinks, granola (cardboard glued together with corn syrup), granola bars (cardboard glued together with corn syrup, pressed into bars and coated with corn syrup), cheese food, cheese whiz…I could go on and on…..
More than 66 percent of Americans are overweight or obese, according to the federal Centers for Disease Control and Prevention, in Atlanta. Although the number of obese women in the United States appears to be holding steady at 33 percent, for most Americans the risk is growing. The nation’s poor diet has long been the scapegoat. There have been proposals to put warning labels on sodas like those on cigarettes. There are calls to ban junk foods from schools. New York and other cities now require restaurants to disclose calorie information on their menus.
But the notion that Americans ever ate well is suspect. In 1966, when Americans were still comparatively thin, more than two billion hamburgers already had been sold in McDonald’s restaurants, noted Dr. Barry Glassner, a sociology professor at the University of Southern California. The recent rise in obesity may have more to do with our increasingly sedentary lifestyles than with the quality of our diets.
But the notion that Americans ever ate well is suspect??? Of course we did, read on….
Here is A Brief History of Nutrition, it will let you see how we have gotten to the “diet” Madness we are at today-
Over the last 90 years we have seen a bewildering array of information on what we should eat. This information has come from any sources; the academic world, the Food and Drug Administration, countless “diet” books. When food “manufacturers” began advertising for the “food” they wanted us to buy, the whole subject became really confusing. We bought into all of it. We went from a diet based on real food which we had eaten throughout time, to breakfast cereals, cookies, candy, processed or instant food. By the 1980’s, 60% of American children’s diets were “non-food”. Manufactured foodstuff, chemicals, and preservatives. Then came fast food, transfats, out sugar intake took a major upswing. The rate of obesity began to climb.
In the mid-1900’s, the academic world, funded by the food processing industry, macronutrients (proteins, fats and carbohydrates) began to loom very large, food quality was pushed to the background and the notion that fats should be limited.
The first to attempt simple dietary guidelines were the dieticians, who came up with the Four Food Groups—meats, poultry, fish and beans; milk and cheeses; vegetables and fruits; and breads and cereals—an innocuous construct that offended no one and completely avoided making any judgments on dietary fats. Emphasis on macronutrient ratios came in with the USDA Food Guide Pyramid in 1992, which reflected the pro-grain conclusions of the McGovern Committee by giving prominence to carbohydrates and relegating animal foods to the smaller areas at the top of the pyramid. Fats and oils are mysteriously put with sweets (which are carbohydrates)—for reasons unknown except to government bureaucrats—and placed at the top of the pyramid with the admonition to "eat sparingly."
Both the US government and the American Heart Association (AHA) now preach fat restriction as the key to good health. Both recommend that less than 30 percent of dietary calories come from fat, with 15 percent from protein and the balance—up to 60 percent—from carbohydrates such as bread, pasta, rice, cereal, fruits and vegetables. (Milk products, nuts and beans are also sources of carbohydrates.)
To the average consumer, these guidelines might seem entirely reasonable.
If we take the governments recommendations on how we should eat the only way to achieve the dietary guidelines with foods that Americans enjoy eating is to drastically reduce meat and fat and pile on the carbs. If we follow this argument to its logical conclusion, we are led to one of two choices—either add lots of sugar to standard American meals or cut way back on animal foods and eat heaps of beans and pasta.
The latter course is the one advocated by extremists like Dean Ornish and John McDougal (and backed by Dr. Neil Barnard of the Physicians’ Committee for Responsible Medicine). Using logic that if a little is good, then even less is better, Ornish and McDougal promote a diet containing only 10 percent of calories as fat, a proposal that makes normal eating impossible. Even nuts are taboo on such a diet. Since beans can contain up to 25 percent protein and have less than 5 percent fat, they are given as the ideal protein source. If you want the complete protein provided by animal foods, your only choices are skim milk, egg whites and shellfish. These diets were invented by academicians, not cooks, and are too unpalatable—not to mention deficient in nutrients—to be taken seriously.
Diets high in carbohydrates and low in fat don’t stick to the ribs. Unimpeded by fats, which have the effect of slowing down digestion, carbohydrate foods flood the bloodstream and quickly raise the blood sugar. Without adequate fat in the diet, the blood sugar is likely to drop shortly thereafter, causing intense hunger and food cravings that are satisfied either by more high-carb foods—or by giving in to fats. Either way, the result is more calories. It’s no coincidence that as Americans have tried to avoid dietary fats; the rate of obesity has climbed. That’s because we’re eating too many calories, say the dieticians, wagging their fingers with disapproval. Unfortunately, only those with iron wills can eat high-carb and low-cal for any length of time. The weak-willed raid the cupboard or the refrigerator, bingeing and splurging on snack foods and sweets.
“The meals we romanticize in the past somehow leave out the reality of what people were eating,” he said. “The average meal had whole milk and ended with pie…. The typical meal had plenty of fat and calories.”
The typical meal had plenty of fat and calories.” DUH!!! Our diets are SUPPOSED to have plenty of calories (about 2000 a day) and plenty of fat (50% of our caloric intake should be from high quality, organic fat)!
“Nostalgia is going to get us nowhere,” he added.
Neither will wishful misconceptions about the efficacy of exercise. First, the federal government told Americans to exercise for half an hour a day. Then, dietary guidelines issued in 2005 changed the advice, recommending 60 to 90 minutes of moderate exercise a day. There was an uproar; many said the goal was unrealistic for Americans. But for many scientists, the more pertinent question was whether such an exercise program would really help people lose weight.
The leisurely after-dinner walk may be pleasant, and it may be better than another night parked in front of the television. But modest exercise of this sort may not do much to reduce weight, evidence suggests.
“People don’t know that a 20-minute walk burns about 100 calories,” said Dr. Madelyn Fernstrom, director of the weight-management center at the University of Pittsburgh Medical Center. “People always overestimate the calories consumed in exercise, and underestimate the calories in food they are eating.”
Exercise has little effect on weight. Don’t get me wrong, it great for a lot of things…cardio-vascular health, muscle fitness and tone, makes you happy, feels great. But to take off 1 pound of body weight you have to burn 3500 calories! Yes…that is a lot of calories. At my weight, 109 pounds, I can run 10 mph, and run for an hour and burn 791 calories in 1 hr. I am not prepared to run 3 1/2 hours a day to take off a pound of body fat…when I can eat perfect, or close to it…and just garden, practice yoga, dance a lot, hula hoop some, ride my bike when I want…and stay in great shape!
I found a site online to do check my body mass index, they say for my height, 5 ft 5, I should weight 130 pounds! Yuck, at even 5 more pounds my waistline thickens (and it’s 24 inches, the same as before I had 5 children!) and I start losing my shape….no way!!!
Tweaking the balance is far more difficult than most people imagine, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University. The math ought to work this way: There are 3,500 calories in a pound. If you subtract 100 calories per day by walking for 20 minutes, you ought to lose a pound every 35 days. Right?
Wrong. First, it’s difficult for an individual to hold calorie intake to a precise amount from day to day. Meals at home and in restaurants vary in size and composition; the nutrition labels on purchased foods — the best guide to calorie content — are at best rough estimates. Calorie counting is therefore an imprecise art.
Second, scientists recently have come to understand that the brain exerts astonishing control over body composition and how much individuals eat. “There are physiological mechanisms that keep us from losing weight,” said Dr. Matthew W. Gilman, the director of the obesity prevention program at Harvard Medical School/Pilgrim Health Care.
Scientists now believe that each individual has a genetically determined weight range spanning perhaps 30 pounds. Those who force their weight below nature’s preassigned levels become hungrier and eat more; several studies also show that their metabolisms slow in a variety of ways as the body tries to conserve energy and regain weight. People trying to exceed their weight range face the opposite situation: eating becomes unappealing, and their metabolisms shift into high gear.
The body’s determination to maintain its composition is why a person can skip a meal, or even fast for short periods, without losing weight. It’s also why burning an extra 100 calories a day will not alter the verdict on the bathroom scales. Struggling against the brain’s innate calorie counters, even strong-willed dieters make up for calories lost on one day with a few extra bites on the next. And they never realize it. “The system operates with 99.6 percent precision,” Dr. Friedman said.
The temptations of our environment — the sedentary living, the ready supply of rich food — may not be entirely to blame for rising obesity rates. In fact, new research suggests that the environment that most strongly influences body composition may be the very first one anybody experiences: the womb.
According to several animal studies, conditions during pregnancy, including the mother’s diet, may determine how fat the offspring are as adults. Human studies have shown that women who eat little in pregnancy, surprisingly, more often have children who grow into fat adults. More than a dozen studies have found that children are more likely to be fat if their mothers smoke during pregnancy.
The research is just beginning, true, but already it has upended some hoary myths about dieting. The body establishes its optimal weight early on, perhaps even before birth, and defends it vigorously through adulthood. As a result, weight control is difficult for most of us. And obesity, the terrible new epidemic of the developed world, is almost impossible to cure.
THIS is the Best ‘They” Can Come Up With??????
They are basically saying obesity is almost impossible to cure? That is just stupidity…plain and simple. Americans eat carbs constantly, they act as if the have the “right” to eat anything they want and expect different results..the definition of neurosis!
The government and big Agra-food companies have sold us a bill of goods, that we need whole grains, that bread is healthy, that cereal is a decent breakfast, that granola bars are healthy…they are wrong; they are just feeding thier pocketbooks, growing the medical and pharmaceutical companies, the cancer “industry”, ….at YOUR expense.
In my career as a nutrition coach, spanning 26 years, I have had 2 different doctors tell me that they were not interested in teaching people to get well to the degree that I teach…that thier patients saw them an average of 7 times a year, and that paid the bills! I had one doctor in Ormond Beach get furious that I taught her best friend how to get rid of systemic yeast…in a month she was yeast free…and this doctor had been treating her for 3 years! And it was her best friend!! And this doctor was a nutritionist!
It’s not that complicated! Eat organic meat, rich meat broths for calcium and iron, healthy organic raw butter and unprocessed coconut oil, lots of low glycemic vegetables (green leafy veggies, mushrooms, onions, peppers, tomatoes) very small amounts of fruits and nuts, healthy organic grass fed or free range meats, organic eggs, small amounts of fermented foods (I make coconut milk yogurt, sauerkraut and kombucha tea).
That’s it, it’s that simple.We have NOT lost the “war” on obesity, we have simply gotten too lazy or too rushed to cook. We have gotten so spoiled by packaged foods that we are ruining our health…and our children’s health…
Filed under: Food and it's Impact on Our Health
For the Overweight, Bad Advice by the Spoonful
By GINA KOLATA in the New York Times
Robyn Beck
And I’m making comments in red….
Two-thirds of Americans are overweight or obese. For most, research shows, neither diets nor moderate exercise brings significant long-term weight loss.
At least they get this right, “diets” don’t work…because people diet by cutting caloric intake, which in turn, cuts nutrient intake…and most people do that while lowering fat and protein intake, thinking it is healthier…it’s not….it only leads to eating carbs (fruits and veggies are 95% carbohydrates)…the body goes into starvation mode, not trusting that you are going to keep eating…and no weight loss occurs. Quite the contrary.
In Brief:
Weight control is not simply a matter of willpower. Genes help determine the body’s "set point," which is defended by the brain.
Health and Weight loss are a matter of cause and effect; our bodies react to what we are doing day to day. I was an extremely unhealthy and fat baby…and now am extremely thin and have been since I was 5 years old. I have had clients who weighed over 500 pounds and through proper nutrition took it off easily and have kept it off…and NOT through caloric restriction…but good solid traditional diet. Your bone size is a set point, it’s not going to change (unless you experience bone loss through poor nutrition)…but fat? Completely controllable through getting off empty carbs and eating enough fat6 and protein to get healthy and maintain perfect weight.
Dieting alone is rarely successful, and relapse rates are high. See above.
Moderate exercise, too, rarely results in substantive long-term weight loss, which requires intensive exercise.
And it takes burning 3500 calories to burn off one pound of body fat. I can run 10 miles at a 10 minute a mile clip and only burn about 450 top 500 calories!
Americans have been getting fatter for years, and with the increase in waistlines has come a surplus of conventional wisdom. If we could just return to traditional diets, if we just walk for 20 minutes a day, exercise gurus and government officials maintain, America’s excess pounds would slowly but surely melt away.
If we could just return to traditional diets they say! YES!!! A diet like your grandmother probably cooked…at least mine did, lots of meat, pan dripping and gravies, rich soups, eggs, lots of greens. But we also had lots of breads and sweets. But it wasn’t every day we had sweets, and when we did they were made with butter or lard (NOT Crisco!). In other words, real food.
When I say a traditional diet, I mean what is traditional for humans going back thousands of years; meat, fat, vegetables, fruits, nuts, herbs… Not stuff out of a box, nothing processed.
Scientists are less sanguine. Many of the so-called facts about obesity, they say, amount to speculation or oversimplification of the medical evidence. Diet and exercise do matter, they now know, but these environmental influences alone do not determine an individual’s weight. Body composition also is dictated by DNA and monitored by the brain. Bypassing these physical systems is not just a matter of willpower.
Body composition is fixed..in other words, I’m never going to be stocky, taller, muscular…but my weight I can control….. and so can everyone else. It’s called choices, making the choice to give up the sodas all day, cookies, cereals, sports drinks, ice cream, corn syrup, McDonalds, 750 calorie lattes, energy drinks, granola (cardboard glued together with corn syrup), granola bars (cardboard glued together with corn syrup, pressed into bars and coated with corn syrup), cheese food, cheese whiz…I could go on and on…..
More than 66 percent of Americans are overweight or obese, according to the federal Centers for Disease Control and Prevention, in Atlanta. Although the number of obese women in the United States appears to be holding steady at 33 percent, for most Americans the risk is growing. The nation’s poor diet has long been the scapegoat. There have been proposals to put warning labels on sodas like those on cigarettes. There are calls to ban junk foods from schools. New York and other cities now require restaurants to disclose calorie information on their menus.
But the notion that Americans ever ate well is suspect. In 1966, when Americans were still comparatively thin, more than two billion hamburgers already had been sold in McDonald’s restaurants, noted Dr. Barry Glassner, a sociology professor at the University of Southern California. The recent rise in obesity may have more to do with our increasingly sedentary lifestyles than with the quality of our diets.
But the notion that Americans ever ate well is suspect??? Of course we did, read on….
Here is A Brief History of Nutrition, it will let you see how we have gotten to the “diet” Madness we are at today-
Over the last 90 years we have seen a bewildering array of information on what we should eat. This information has come from any sources; the academic world, the Food and Drug Administration, countless “diet” books. When food “manufacturers” began advertising for the “food” they wanted us to buy, the whole subject became really confusing. We bought into all of it. We went from a diet based on real food which we had eaten throughout time, to breakfast cereals, cookies, candy, processed or instant food. By the 1980’s, 60% of American children’s diets were “non-food”. Manufactured foodstuff, chemicals, and preservatives. Then came fast food, transfats, out sugar intake took a major upswing. The rate of obesity began to climb.
In the mid-1900’s, the academic world, funded by the food processing industry, macronutrients (proteins, fats and carbohydrates) began to loom very large, food quality was pushed to the background and the notion that fats should be limited.
The first to attempt simple dietary guidelines were the dieticians, who came up with the Four Food Groups—meats, poultry, fish and beans; milk and cheeses; vegetables and fruits; and breads and cereals—an innocuous construct that offended no one and completely avoided making any judgments on dietary fats. Emphasis on macronutrient ratios came in with the USDA Food Guide Pyramid in 1992, which reflected the pro-grain conclusions of the McGovern Committee by giving prominence to carbohydrates and relegating animal foods to the smaller areas at the top of the pyramid. Fats and oils are mysteriously put with sweets (which are carbohydrates)—for reasons unknown except to government bureaucrats—and placed at the top of the pyramid with the admonition to "eat sparingly."
Both the US government and the American Heart Association (AHA) now preach fat restriction as the key to good health. Both recommend that less than 30 percent of dietary calories come from fat, with 15 percent from protein and the balance—up to 60 percent—from carbohydrates such as bread, pasta, rice, cereal, fruits and vegetables. (Milk products, nuts and beans are also sources of carbohydrates.)
To the average consumer, these guidelines might seem entirely reasonable.
If we take the governments recommendations on how we should eat the only way to achieve the dietary guidelines with foods that Americans enjoy eating is to drastically reduce meat and fat and pile on the carbs. If we follow this argument to its logical conclusion, we are led to one of two choices—either add lots of sugar to standard American meals or cut way back on animal foods and eat heaps of beans and pasta.
The latter course is the one advocated by extremists like Dean Ornish and John McDougal (and backed by Dr. Neil Barnard of the Physicians’ Committee for Responsible Medicine). Using logic that if a little is good, then even less is better, Ornish and McDougal promote a diet containing only 10 percent of calories as fat, a proposal that makes normal eating impossible. Even nuts are taboo on such a diet. Since beans can contain up to 25 percent protein and have less than 5 percent fat, they are given as the ideal protein source. If you want the complete protein provided by animal foods, your only choices are skim milk, egg whites and shellfish. These diets were invented by academicians, not cooks, and are too unpalatable—not to mention deficient in nutrients—to be taken seriously.
Diets high in carbohydrates and low in fat don’t stick to the ribs. Unimpeded by fats, which have the effect of slowing down digestion, carbohydrate foods flood the bloodstream and quickly raise the blood sugar. Without adequate fat in the diet, the blood sugar is likely to drop shortly thereafter, causing intense hunger and food cravings that are satisfied either by more high-carb foods—or by giving in to fats. Either way, the result is more calories. It’s no coincidence that as Americans have tried to avoid dietary fats; the rate of obesity has climbed. That’s because we’re eating too many calories, say the dieticians, wagging their fingers with disapproval. Unfortunately, only those with iron wills can eat high-carb and low-cal for any length of time. The weak-willed raid the cupboard or the refrigerator, bingeing and splurging on snack foods and sweets.
“The meals we romanticize in the past somehow leave out the reality of what people were eating,” he said. “The average meal had whole milk and ended with pie…. The typical meal had plenty of fat and calories.”
The typical meal had plenty of fat and calories.” DUH!!! Our diets are SUPPOSED to have plenty of calories (about 2000 a day) and plenty of fat (50% of our caloric intake should be from high quality, organic fat)!
“Nostalgia is going to get us nowhere,” he added.
Neither will wishful misconceptions about the efficacy of exercise. First, the federal government told Americans to exercise for half an hour a day. Then, dietary guidelines issued in 2005 changed the advice, recommending 60 to 90 minutes of moderate exercise a day. There was an uproar; many said the goal was unrealistic for Americans. But for many scientists, the more pertinent question was whether such an exercise program would really help people lose weight.
The leisurely after-dinner walk may be pleasant, and it may be better than another night parked in front of the television. But modest exercise of this sort may not do much to reduce weight, evidence suggests.
“People don’t know that a 20-minute walk burns about 100 calories,” said Dr. Madelyn Fernstrom, director of the weight-management center at the University of Pittsburgh Medical Center. “People always overestimate the calories consumed in exercise, and underestimate the calories in food they are eating.”
Exercise has little effect on weight. Don’t get me wrong, it great for a lot of things…cardio-vascular health, muscle fitness and tone, makes you happy, feels great. But to take off 1 pound of body weight you have to burn 3500 calories! Yes…that is a lot of calories. At my weight, 109 pounds, I can run 10 mph, and run for an hour and burn 791 calories in 1 hr. I am not prepared to run 3 1/2 hours a day to take off a pound of body fat…when I can eat perfect, or close to it…and just garden, practice yoga, dance a lot, hula hoop some, ride my bike when I want…and stay in great shape!
I found a site online to do check my body mass index, they say for my height, 5 ft 5, I should weight 130 pounds! Yuck, at even 5 more pounds my waistline thickens (and it’s 24 inches, the same as before I had 5 children!) and I start losing my shape….no way!!!
Tweaking the balance is far more difficult than most people imagine, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University. The math ought to work this way: There are 3,500 calories in a pound. If you subtract 100 calories per day by walking for 20 minutes, you ought to lose a pound every 35 days. Right?
Wrong. First, it’s difficult for an individual to hold calorie intake to a precise amount from day to day. Meals at home and in restaurants vary in size and composition; the nutrition labels on purchased foods — the best guide to calorie content — are at best rough estimates. Calorie counting is therefore an imprecise art.
Second, scientists recently have come to understand that the brain exerts astonishing control over body composition and how much individuals eat. “There are physiological mechanisms that keep us from losing weight,” said Dr. Matthew W. Gilman, the director of the obesity prevention program at Harvard Medical School/Pilgrim Health Care.
Scientists now believe that each individual has a genetically determined weight range spanning perhaps 30 pounds. Those who force their weight below nature’s preassigned levels become hungrier and eat more; several studies also show that their metabolisms slow in a variety of ways as the body tries to conserve energy and regain weight. People trying to exceed their weight range face the opposite situation: eating becomes unappealing, and their metabolisms shift into high gear.
The body’s determination to maintain its composition is why a person can skip a meal, or even fast for short periods, without losing weight. It’s also why burning an extra 100 calories a day will not alter the verdict on the bathroom scales. Struggling against the brain’s innate calorie counters, even strong-willed dieters make up for calories lost on one day with a few extra bites on the next. And they never realize it. “The system operates with 99.6 percent precision,” Dr. Friedman said.
The temptations of our environment — the sedentary living, the ready supply of rich food — may not be entirely to blame for rising obesity rates. In fact, new research suggests that the environment that most strongly influences body composition may be the very first one anybody experiences: the womb.
According to several animal studies, conditions during pregnancy, including the mother’s diet, may determine how fat the offspring are as adults. Human studies have shown that women who eat little in pregnancy, surprisingly, more often have children who grow into fat adults. More than a dozen studies have found that children are more likely to be fat if their mothers smoke during pregnancy.
The research is just beginning, true, but already it has upended some hoary myths about dieting. The body establishes its optimal weight early on, perhaps even before birth, and defends it vigorously through adulthood. As a result, weight control is difficult for most of us. And obesity, the terrible new epidemic of the developed world, is almost impossible to cure.
THIS is the Best ‘They” Can Come Up With??????
They are basically saying obesity is almost impossible to cure? That is just stupidity…plain and simple. Americans eat carbs constantly, they act as if the have the “right” to eat anything they want and expect different results..the definition of neurosis!
The government and big Agra-food companies have sold us a bill of goods, that we need whole grains, that bread is healthy, that cereal is a decent breakfast, that granola bars are healthy…they are wrong; they are just feeding thier pocketbooks, growing the medical and pharmaceutical companies, the cancer “industry”, ….at YOUR expense.
In my career as a nutrition coach, spanning 26 years, I have had 2 different doctors tell me that they were not interested in teaching people to get well to the degree that I teach…that thier patients saw them an average of 7 times a year, and that paid the bills! I had one doctor in Ormond Beach get furious that I taught her best friend how to get rid of systemic yeast…in a month she was yeast free…and this doctor had been treating her for 3 years! And it was her best friend!! And this doctor was a nutritionist!
It’s not that complicated! Eat organic meat, rich meat broths for calcium and iron, healthy organic raw butter and unprocessed coconut oil, lots of low glycemic vegetables (green leafy veggies, mushrooms, onions, peppers, tomatoes) very small amounts of fruits and nuts, healthy organic grass fed or free range meats, organic eggs, small amounts of fermented foods (I make coconut milk yogurt, sauerkraut and kombucha tea).
That’s it, it’s that simple.We have NOT lost the “war” on obesity, we have simply gotten too lazy or too rushed to cook. We have gotten so spoiled by packaged foods that we are ruining our health…and our children’s health…
September 2, 2009
The 4 or 5-digit number that you’ll find on the little sticker on your produce is a Price Look-Up, or PLU, code. They’ve been used by grocery stores for about 20 years to identify produce for pricing at the cash register. (I always did wonder how grocery clerks could spot the difference between Bosc and Bartlett pears on sight.) These days, the International Federation for Produce Standards (IFPS), a voluntary organization of those associated with the fresh produce industry, coordinates the use of standardized codes throughout the world.
PLU codes are used for fruits and vegetables sold individually and for other items like nuts and dried fruit sold in bulk. (You won’t see a PLU code on anything with a fixed weight, like a pint of blueberries, or that’s been processed, like a fruit salad or juice.) The code signals to the retailer the information needed to determine the price – so “4131″ indicates not only the type of fruit (“apple”) but also the variety (“Fuji”) and even the size (“extra large”). If you’re a produce nerd like me, you can even look up the exact variety of what you’re eating on the IFPS website.
Organic & GMO
As you’re no doubt well aware, organic or not factors into the price of what you’re buying. As a result, the IFPS decided that organic produce would be identified with a “9″ in front of the standard 4 digits traditionally used for the fruit or veggie. So if that big Fuji is organic, the code won’t just be “4131″ but “94131.”
Similarly, an “8″ as the first of a five-digit code indicates genetically-modified produce. If that Fuji was created using GM technology, the code would be “84131.”
Retailer Codes, not Regulations
Keep in mind that these codes are administered by a voluntary organization (the International Federation for Produce Standards) that’s made up largely of produce trade associations. Their main purpose is not to inform consumers but to facilitate grocery transactions.
Produce advertised as organic must comply with the standards of the USDA National Organic Program, but there are no labeling requirements for genetically-modified foods. No need to get too worried about looking for number 8’s, though: given current technology, there is very little PLU-coded produce that would have been genetically engineered. Thought there’s plenty of GMO corn and soybeans out there, GM technology hasn’t yet made inroads on the individually-sold fruits and veggies like tomatoes, apples, etc.
The awesome image (that was) above is by Artist Cheri Kopp; see more of her work at- http://www.cherikopp.com/index.html She wanted me to take it down, but you should check out her work…
