POSTED ON 8 DECEMBER 2010 BY BRODRICK KENT

How can you eat all the fat and grease that you want and still lose weight? Humans are primates; genetically and structurally, we closely resemble the gorilla. We are designed, just like the other large primates, to survive predominantly on plant foods rich in carbohydrates.

When the human body finds that it does not have enough carbohydrates to run its "machinery" properly, it produces ketones, an emergency fuel that can be utilized in times of crisis.

At rest, the brain consumes about 80 percent of our energy needs. Under normal conditions, the brain can utilize only glucose as fuel. However, the human organism has evolved a remarkable adaptation that enables it to survive for long periods of time without food.

In the first few days of no carbohydrate fuel (food), the body's glucose reserves dwindle and the only way we can produce enough fuel for our hungry brain is by breaking down muscle tissue to manufacture glucose. Glucose cannot be manufactured from fat. Fortunately, our body has a built-in mechanism that allows us to conserve our muscle tissue by metabolizing a more efficient energy source--our fat supply.

After a day or two of not eating, the body dips into its fats reserves to produce ketones as an emergency fuel. As the level of ketones rise in our bloodstream, the brain accepts ketones as an alternative fuel. In this manner, we conserve muscle and increase survival during periods of food deprivation.

Atkins' dietary recommendations prey on his survival mechanism. When we restrict carbohydrates so markedly, the body thinks we care calorically deprived and ketosis results. The body begins to lose fat, even if we are consuming plenty of high-fat foods, as Atkins recommends. Once you start consuming carbohydrate-containing fruits, vegetables, or beans, the ketosis ends and the meat and fat become fattening again. Meat consumption leads to weigh gain, unless you have caused a carbohydrate-deficiency ketosis.

To make matters even worse, you pay an extra penalty from a diet so high in fat and protein to generate a chronic ketosis. Besides the increased cancer risk, your kidneys are placed under greater stress and will age more rapidly. It can take many, many years for such damage to be detected by blood tests. By the time the blood reflects the abnormality, irreversible damage may have already occurred. Blood tests that monitor kidney function typically do not begin to detect problems until more than 90 percent of the kidneys have been destroyed.

Protein is metabolized in the liver, and the nitrogenous wastes generated are broken down and then excreted by the kidney. These wastes must be eliminated for the body to maintain normal purity and a stable state of equilibrium. Most doctors are taught in medial school that a high-protein diet ages the kidney.(1) What has been accepted as the normal age-related loss in renal function may really be a cumulative injury secondary to the heavy pressure imposed on the kidney by our high-protein eating habits.(2)

By the eighth decade of life, Americans lost about 30 percent of their kidney function.(3) Many people develop kidney problems at young ages under the high-protein stress. Low-protein diets are routinely used to treat patients with liver and kidney failure.(4) A recent multitrial analysis showed that reducing protein intake for patients with kidney disease decreased kidney-related death by about 40 percent.(5)

Diabetics, who are at increased risk of kidney disease, are extremely sensitive to the stresses a high-protein diet place on the kidney.(6) In a large, multicentered study involving 1,521 patients, most of the diabetics who ate too much animal protein had lost over half their kidney function, and almost all the damage was irreversible.(7) In my practice, I have seen numerous patients who have experienced significant worsening of their kidney function after attempting weight loss and diabetic control with high protein diets. Coincidence? I think not. Damage from such lopsided nutritional advice can be very serious.

Ketogenic diets, like Atkins, have been used to treat children with seizure disorders when medication alone is unresponsive. Medical studies reveal that these diets can result in serious health consequences. Investigators report a greater potential for adverse events than had ever been anticipated. The dangers of these high-protein diets include hemolytic anemia, abnormal liver function, renal tubular acidosis, and spontaneous bone fractures (despite calcium supplementation).(8) Kidney stones are another risk of high protein diets.(9) These studies point out that there are many subtle adverse outcomes not being attributed to this dangerous way of eating. One outcome is the Atkins Diet's relative inability to lower cholesterol when compared to my vegetable-based, nutrient-dense diet-style.

By Dr. Joel Fuhrman MD 'Eat to Live'

1. Kasiske, B.L., J.D. Lakatua, J.Z. Ma, and T.A. Louis. 1998. A meta-analysis of the effects of dietary protein restriction on the rate of decline of renal function. Am. J. Kidney Dis. 31 (6): 954-61; Holm, E.A., and K. Solling. 1996. Dietary protein restriction and progression of chronic renal insufficiency: a review of literature. J. Intern. Med. 239 (2): 99-104.
2. Brenner, B.M., T.W. Meyer, and T.H. Hostetter. 1982. Dietary protein intake and the progressive nature of kidney disease: the role of the hemodynamically mediated glomerular injury in the pathogensis of progressive glomerular sclerosis in aging, renal ablation and intrinsic renal disease. N. Eng. J. Med. 307 (11): 652-59.
3. Clark, B. 2000. Biology of renal aging in humans. Adv. Ren. Replace. Ther. 7 (1): 11-21.
4. Rosman, J.B. 1995. Protein restriction in diet therapy in chronic kidney insufficiency. Ther. Umsch. 52 (8): 515-18; Zeller, K.R. 1991. Low-protein diets in renal disease. Diabetes care 14 (9): 856-66.
5. Fouque, D., P. Wang, M. Laville, and J.P. Boissel. 2000. Low protein diets delay end-stage renal disease in non-diabetic adults with chronic renal failure. Nephrol. Dial. Transplant 15 (12): 1986-92.
6. Gin, H., V. Rigalleau, and M. Aparicio. 2000. Lipids, protein intake, and diabetic nephropathy. Diabetes Metab. 26 (supp. 4): 45-53.
7. Pedrini, M.T., A.S. Levey, J. Lau, T.C. Chalmers, and P.H. Wang. 1996. The effect of dietary protein on the progression of diabetic and nondiabetic renal disease: a meta-analysis. Ann. Intern. Med. 124 (7): 627-32.
8. Bankhead, C. 1998. Ketogenic diet can cause serious adverse effects, data suggests. Medical Tribune 39 (17): 23.
9. Licata, A.A., E. Bow, F.C. Bartler, et al. 1979. Effect of dietary protein on urinary calcium in normal subjects and in patients with nephrolithiasis. Metabolism 28: 895; Robertson, W.G., P.J. Heyburn, M. Peacock, et al. 1979. The effect of high animal protein intake on the risk of calcium stone formation in the urinary tract. Clin. Sci. 57: 285; Brokis, J.G., A.S. Levitt, and S.M. Cruthers. 1982, The effect of vegetable and animal protein diet on calcium, urate and oxalate excretion. Br. J. Urol. 54: 590; Robertson, W.G., M. Peacock, P.J. Heyburn, et al. 1981. The risk of calcium stone formation in relation to affluence and dietary animal protein, in Brokis, J.G., and B. Finlayson, eds. Urinary calculus, International Urinary Stone Conference. Littleton, Colo.: PSG Publishing, p. 3.