You’d think that Dr. Bray being a doctor (who probably is a statinator) would realize that statins have 11 other very strong effects besides mere cholesterol lowering.

You’d think he could figure out that non – statin cholesterol lowering trials have been complete failures for reducing CAD deaths. And that dietary cholesterol lowering clinical intervention trials also have been failures. You’d think he’d take note of the JUPITER and ENHANCE trials. You’d also think he would know (as Dr. Uffe Ravnskov points out ) there is no dose response with statins.

You’d think he’d realize any ( slight ) reduction in CAD deaths amoung patients WITH CAD from the use statin drugs is enitrely due to these 11 effects , epsecially in light of the above mentioned evidence.

It really amazes me just how many doctors can’t seem to grasp that just because statin drugs (which lower cholesterol, but also do a myriad of other things ) lower CAD death rates amoung patients WITH CAD a little bit, doesn’t mean cholesterol lowering is the mechanism. They can’t seem to seperate mere cholesterol reduction from the use of statin drugs. Cholesterol lowering trials using non statin drugs (which have no pleotropic effects) and their lack of benefit should make this blatantly obvious to them , you would think.

For example The Lipid Research Clinics Coronary Primary Prevention Trial found that out of 3,086 pateints those taking cholestyramine had 30 CAD deaths vs 38 in the controls. Total mortality was 68 in the treatment group vs 71 in the controls. Another non – supportive result amoung many for the cholesterol theory proponents.

If anything statin drugs strongly challange the lipid hypothesis.

Take Care,

Razwell

I gave up on dieting because I was so hungry and so tired all the time. I couldn’t adhere to a lowfat or calorie restricted diet very long. When I started eating fewer carbs the constant hunger went away, my appetite was cut in half.

I read “Dr. Neal Barnard’s Program for Reversing [type II] Diabetes”, in which he focusses on the role of fat stored in muscle cells in causing insulin resistance in individuals who have a tendancy to store fat in their muscle cells (who also tend to have relatives with type II diabetes). This can lead to the whole metabolic syndrome spiral. He has clinical trial results that show his good carbs, VERY low-fat vegan diet with exercise is effective for weight loss, improved insulin sensitivity and improved cholesterol.

In the other corner is Dr. Richard Bernstein, whose “[type I or II] Diabetes Solution” involves “a low carbohydrate diet and exercise”. There are studies that support his approach for weight loss, blood sugar control, and improved blood lipids.

So there is more than one way to skin a cat. When Bray says “Weight loss is related to adherence to the diet, not to its macronutrient composition.” he is rolls several valid ideas into that one statement, but misses issues that statement does not address. Like — what influences adherence to the diet, do some diets just make weight loss more difficult, and why can’t everyone lose weight on a Michael Phelps diet?

Assuming the ‘insulin connection’ is dealt with, what can an obese (Or FORMERLY obese) person do to NATURALLY increase his/her leptin sensitivity?

I would expect that time at the new lower weight would help, but I don’t know for sure. I don’t think the issue has been studied. And I would make sure to keep my triglycerides low so that the leptin I did have could easily get into my brain.

Exactly. I’m sure that a defense of his own career is the least of Dr. Bray’s conflicts of interest. Just one more pseudoscientist in the pocket of larger interests.

We do now. Thanks. At least is wasn’t ‘reknowned.’

MRE

Hey Doc–

MRE

When you give leptin to weight reduced people they can maintain weight much more easily.

An article about a study in june which demonstrates leptin allows people to maintain weight after a diet

I speak not only hypothetically but from personal experience. I have lost over 100% of my body weight. This has left me with a leptin level that is almost non-existent and I have all symptoms of leptin deficiency (other than obesity, of course). I am pariticpating in a study for hypothalamic amenorrhea which involves leptin replacement. Since starting a very low dose leptin all of my symptoms (including infertility) are much, much better! I feel like a normal weight person, it is very easy to eat normal calories, my glucose tolerance is better (less hypoglycemia) and I have so much more energy. I have had menses again when I haven’t had them in four years (after all the weight loss).

Don’t get me wrong – a low carb diet (like protein power) is essential to STOP obesity, and to reduce weight… but this obesity thing is a lot more complex and permanent than insulin stuffing food in fat cells. I believe that insulin damages the fat tissue, possibly because insulin makes too many fat cells grow in morbid obesity (sort of like a tumor). Google “insulin adipocyte hyperplasia”.
Because of how insulin changes the fat tissue permanently, dieting alone will not allow you to maintain a low fat mass normally (i.e. without metabolic consequences). Your depleted fat tissue will behave as if starving because the glut of depleted fat cells does not make leptin normally (even if your absolute fat mass is within a healthy range, your number of fat CELLs are not in normal range so you have a whole lot of small fat cells that act as if starving).

This is not something I”m making up… I actually had blood tests and it was all verified. My leptin level was extremely low.

Low carb will bring your insulin down and stop the disease process.
However, once developed, obesity is intractable because insulin changes the body and fat tissue in such a way that a high weight becomes “normal” weight. Leptin supplementation is a major, major part in allowing the previously obese to achieve a normal weight without starvation symptoms.