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The material presented on this site comes from individuals with years of hard-won experience either practicing alternative diets or observing those who do. As you'll find, no two writers will necessarily agree on all topics. A unifying theme, however, is the intent to squarely acknowledge and discuss the sometimes serious problems that can occur on alternative diets but often go unreported, and to go beyond the simplistic dogmas readily available elsewhere--in fact almost everywhere--to "explain them away." A sense of admirable idealism is often a motivating factor encouraging people to take responsibility for their own health and to explore different diets. However, the development of emotional attachments to philosophies underlying such diets can often end up becoming far more important for some individuals than the results they obtain--or fail to. One result has been widespread refusal in the alternative diet community to face health and behavioral problems that may arise on these diets. A common thread in what you'll read here is that a kind of subjective, "blinded naturalism" has become more or less endemic in the vegetarian, raw-food, and alternative diet movements, which can lead to serious health troubles.

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"(NaturalNews) New research published in The Journal of the Federation of American Societies for Experimental Biology (FASEB) has found that the "Western" diet, typically high in sugar and fat, may be responsible for activating genes that signal the body to become fatter. According to scientists, the body's response to high amounts of energy-dense food is to activate the kappa opioid receptor which triggers increased fat storage. Researchers arrived at this conclusion by conducting an experiment on two groups of mice. One group had its kappa opioid receptors genetically deactivated while the other remained intact. Both groups were fed diets high in fat and sugar for 16 weeks. At the end of 16 weeks, the group with the deactivated receptor remained lean while the control group gained significant weight. Besides limiting their bodies' ability to store energy-dense food in their fat stores, the mice whose receptors had been deactivated were noted to also have a limited ability to assimilate and store nutrients from the foods they ingested. Traci Ann Czyzyk-Morgan, one of the study's researchers, indicated that the findings prove the hypothesis long held by many in the scientific community that the kappa opioid receptor may be responsible for causing widespread obesity in Western countries. She and others continue to encourage people to avoid diets high in fat and sugar. "

Consumption of cod and weight loss in young overweight and obese adults on an energy reduced diet for 8-weeks. Ramel A, Jonsdottir MT, Thorsdottir I. Nutr Metab Cardiovasc Dis. 2009 Dec;19(10):690-6. Epub 2009 Apr 8. PMID: 19356912 Conclusion A dose-response relationship between cod consumption and weight loss during an 8-week energy restriction diet is found and 5×150g cod/week results in 1.7kg greater weight loss in young overweight or obese adults than a isocaloric diet without seafood

If you want to reduce your risk for getting cancer, heart disease, diabetes and a host of other diseases, the message is clear - eat a nutrient-rich, low-fat, high fiber diet, with plenty of fruit and vegetables. So why is this wisdom forgotten when a person is diagnosed with cancer, and the standard advice becomes: "Eat whatever you want, whatever you can tolerate," even when this may include a diet high in fat and refined sugars. \n\nAccording to two of the country's leading authorities on cancer and nutrition, David Katz, MD and Keith Block, MD, the typical American high-fat, empty calorie diet can set the stage for an inflammatory response that actually fuels a cancer patient's disease, undermines treatment, and promotes malnutrition.

"Tuesday, July 8, 2008 Wheat is Invading China Dr. Michael Eades linked to an interesting study yesterday on his Health and Nutrition blog. It's entitled "Vegetable-Rich Food Pattern is Related to Obesity in China." It's one of these epidemiological studies where they try to divide subjects into different categories of eating patterns and see how health problems associate with each one. They identified four patterns: the 'macho' diet high in meat and alcohol; the 'traditional' diet high in rice and vegetables; the 'sweet tooth' pattern high in cake, dairy and various drinks; and the 'vegetable rich' diet high in wheat, vegetables, fruit and tofu. The only pattern that associated with obesity was the vegetable-rich diet. The 25% of people eating closest to the vegetable-rich pattern were more than twice as likely to be obese as the 25% adhering the least. The authors of the paper try to blame the increased obesity on a higher intake of vegetable oil from stir-frying the vegetables, but that explanation is juvenile and misleading. A cursory glance at table 3 reveals that the vegetable-eaters weren't eating any more fat than their thinner neighbors. Dr. Eades suggests that their higher carbohydrate intake (+10%) and higher calorie intake (+120 kcal/day) are responsible for the weight gain, but I wasn't satisfied with that explanation so I took a closer look.

An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women. Volek JS, Sharman MJ, Gómez AL, Scheett TP, Kraemer WJ. J Nutr. 2003 Sep;133(9):2756-61. PMID: 12949361

Eggs modulate the inflammatory response to carbohydrate restricted diets in overweight men. Ratliff JC, Mutungi G, Puglisi MJ, Volek JS, Fernandez ML. Nutr Metab (Lond). 2008 Feb 20;5:6. PMID: 18289377 Carbohydrate restricted diets (CRD) consistently lower glucose and insulin levels and improve atherogenic dyslipidemia [decreasing triglycerides and increasing HDL cholesterol (HDL-C)]. We have previously shown that male subjects following a CRD experienced significant increases in HDL-C only if they were consuming a higher intake of cholesterol provided by eggs compared to those individuals who were taking lower concentrations of dietary cholesterol. Here, as a follow up of our previous study, we examined the effects of eggs (a source of both dietary cholesterol and lutein) on adiponectin, a marker of insulin sensitivity, and on inflammatory markers in the context of a CRD. Conclusion A CRD with daily intake of eggs decreased plasma CRP and increased plasma adiponectin compared to a CRD without eggs. These findings indicate that eggs make a significant contribution to the anti-inflammatory effects of CRD, possibly due to the presence of cholesterol, which increases HDL-C and to the antioxidant lutein which modulates certain inflammatory responses.

In response to the Heart Scan Blog post, Post-Traumatic Grain Disorder, Anne commented: While on the American Heart Association diet my lipids peaked in 2003. I even tried the Ornish diet for a short time, but found it impossible. Total Cholesterol: 201 Triglycerides: 263 HDL: 62 LDL: 86 After I stopped eating gluten (I am very sensitive), my lipid panel improved slightly. This past year I started eating to keep my blood sugar under control by eliminating sugars and other grains. Now this is my most recent lab: Total Cholesterol: 162 Triglycerides: 80 HDL: 71 LDL: 75

"In an article published in the December 29, 2005, issue of the journal Cell, the researchers report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production. Importantly, the scientists showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells. "We have discovered a mechanistic explanation for beta cell failure in response to a high-fat diet and obesity, a molecular trigger which begins the chain of events leading from hyperglycemia to insulin resistance and type 2 diabetes," said Jamey Marth, a Howard Hughes Medical Institute investigator at the University of California, San Diego (UCSD). Marth and first author Kazuaki Ohtsubo at UCSD collaborated on the studies with researchers from the Kirin Brewery Co. Ltd., and the University of Fukui, both in Japan."

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Immunologic effects of national cholesterol education panel step-2 diets with and without fish-derived N-3 fatty acid enrichment. Meydani SN, Lichtenstein AH, Cornwall S, Meydani M, Goldin BR, Rasmussen H, Dinarello CA, Schaefer EJ. J Clin Invest. 1993 Jul;92(1):105-13. PMID: 8325975 doi:10.1172/JCI116537 the low-fat, high-fish diet significantly decreased the percentage of helper T cells whereas the percentage of suppressor T cells increased

Floyd Chilton and colleagues wanted to examine whether theses fatty acids might have other effects, and developed a dietary intervention strategy in which 27 healthy humans were fed a controlled diet mimicking the w6/w3 ratios of early humans over 5 weeks. They then looked at the gene levels of immune signals and cytokines (protein immune messengers), that impact autoimmunity and allergy in blood cells and found that many key signaling genes that promote inflammation were markedly reduced compared to a normal diet, including a signaling gene for a protein called PI3K, a critical early step in autoimmune and allergic inflammation responses. This study demonstrates, for the first time in humans, that large changes in gene expression are likely an important mechanism by which these omega fatty acids exert their potent clinical effects

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Calorie-restricted diets are thought to protect against cancer and slow tumor growth, and a new study published in this week's Nature begins to tease out why the measure works for some tumors, and not for others. For almost a century, researchers have known that fasting helps animals live longer and avoid some cancers, "but which type of cancers would be amenable to this approach, from a therapeutic standpoint, is still an open question," said Pier Paolo Pandolfi, a cancer geneticist at Harvard Medical School and Beth Israel Deaconess Cancer Center in Boston, Mass., who was not involved in the study. The study is exciting because it is one of the first to start answering that question at the genetic level, he said.

Dr. Staffan Lindeberg has published a new study using the "paleolithic diet" to treat type II diabetics (free full text). Type II diabetes, formerly known as late-onset diabetes until it began appearing in children, is typically thought to develop as a result of insulin resistance (a lowered tissue response to the glucose-clearing function of insulin). This is often followed by a decrease in insulin secretion due to degeneration of the insulin-secreting pancreatic beta cells. After Dr. Lindeberg's wild success treating patients with type II diabetes or glucose intolerance, in which he normalized the glucose tolerance of all 14 of his volunteers in 12 weeks, he set out to replicate the experiment. This time, he began with 13 men and women who had been diagnosed with type II diabetes for an average of 9 years.

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Over acidity has been studied by many scientists as you will see here. You can help prevent the negative side effects by eating plenty of green foods and drinking green alkalizing drinks Excessive dietary intake of protein with consequent increase in metabolic acid production result in compensatory mechanisms that lead to progression of kidney stones, bone disease, renal disease and a catabolic state. Chronic metabolic acidosis is a process whereby an excess acid load is placed on the body due to excess acid generation or diminished acid removal by normal homeostatic mechanisms. Excessive meat ingestion and aging are two clinical conditions often associated with chronic metabolic acidosis. The body's homeostatic response to this pathology is very efficient. Therefore, the blood pH is frequently maintained within the "normal" range. However, these homeostatic responses engender pathologic consequences such as nephrolithiasis, bone demineralization, muscle protein breakdown and renal growth.

"November 26, 2008 New evidence may explain why it is that we lose not only our youthful looks, but also our youthful pattern of gene activity with age. A report in the November 26th issue of the journal Cell, a Cell Press publication, reveals that a protein perhaps best known for its role in the life-extending benefits of a low-calorie diet also maintains the stability of the mammalian genome-the complete set of genetic instructions "written" in DNA. The researchers found in studies of mammalian stem cells that the protein SIRT1 controls the packaging of DNA into chromatin, thereby setting the youthful pattern of gene activity by keeping select genes switched off. In response to DNA damage, those SIRT1 proteins leave their posts to go off and assist in the necessary repairs. That change in SIRT1's job description leads to shifts in gene activity that parallel those seen in the aging mouse brain, they show. They suspect similar changes would also be found in other body tissues as well."