When I cheat, though, I get them bad… exactly 2 nights later. Perhaps the serotonin drop off that follows the spike?

Hi Keenan–

Thanks for relating your experience.  I guess I’ll need to read up a little on inositol.

Cheers–

MRE 

I have ALWAYS questioned the anti saturated fat campaign , just from the way a low saturated fat meal made me feel. Very hungry . bad mood , completely unsatisfied. I ALWAYS felt like crap after skim milk

On the other hand berries and red meat , grass fed (the way nature intended with the n3 n6 ratios balanced) has me feeling great

I always felt like crap after skim milk.

I can’t believe anyone would be taken by this type of a “grasping at straws attempt to explain the cause of CHD”. Nature sure does not evolve to kill itself off. Saturated fat was available to our ancestors and they sure ate it. Along with leafy greens nuts fruits.

To rail against a natural and healthy food source is beyond dumb. I mean its basic intelligence example – do Lipid Hypothesis proponents really think Bear Grylles would survive in the wilderness with no saturated fat and protein? Lipid Hypothesis proponents INVENT “paradoxes” and ignore the evidence of the Maasai, Dinkas , Samburu , French, Inuits , Tokeluans and many more .

Take Care,

Razwell

Hi Razwell–

You’re preaching to the choir.

Cheers–

MRE 

I found this link through the fasting yahoo group. Apparently, it references an article in the same issue, December 2006. I’ve been following a 19-hour fasting plan and was rather dismayed to read about IGF levels increasing with low carb, as I follow very low carb myself, under about 40 grams per day. Any comments you have about this research would be welcome! Again, it appears to be referencing the same journal of clinic nutrition, December 2006.

Thanks.

http://www.hon.ch/News/HSN/536486.html

Hi Jill–

A couple of things…

First, this report states that high levels of IGF-1 increase the growth of cancers that are already in place. At no point does it posit that IGF-1 causes the cancers in the first place. I would bet that a good quality low-carb diet, especially one followed on an intermittent fasting schedule would reduce the incidence of cancer formation, so the levels of IGF-1 are immaterial.

Second, there is free IGF-1 and bound IGF-1. And there is a world of difference between the two. Free IGF-1 is the active hormone whereas bound IGF-1 in inactive. When one measures total IGF-1 levels one gets the sum of both the free and the bound hormone, which tells very little about what’s going on.  I haven’t looked at this paper in a while (and don’t have access to it right now since I’m traveling), but as I recall the researchers measured total IGF-1, not free IGF-1.

Chronically elevated insulin levels as are found in those following high-carb diets cause the liver to make LESS IGFBP (IGF binding protein), meaning that there will usually be more free IGF circulating since there is less IGFBP for it to bind to.  This can lead to the situation where the total IGF-1 is low, but the free IGF-1 is high.  A low-carb diet that leads to less insulin drives the liver to synthesis MORE IGFBP, which means more bound and less free IGF-1.  This is a condition in which the total IGF-1 is high, but the free (or active) IGF-1 is actually low.

I hope this clarifies things.

Cheers–

MRE 

I have researched the Vitamin C connection for the past 5 years and believing in it have followed the Linus Pauling recommendations and have taken between 10 and 20 gms per day together with 4 gm l-lysine and 1gm l-proline. I do also take a broad spectrum of other suppliment nutrients, following a MI in Feb. 2002. Blood tests, ecg, and echocardiogram confirmed. Angiogram showed complete blockage at bottom of LAD and 40% mid vessel in RCA. Over a period of 1 – 2 years all signs of MI resolved and I am now told following echo and ecg that my heart is normal function and that performance at ecg is that of a young fit person (14 mins 40 secs. standard Bruce test) with no deviations. I am 63 yrs. next month. I was initially on the usual meds. of Beta blocker, Ace Inhibitor, Plavix, Aspirin, Lipitor (10mg). All the meds. were the minimal doses. I have been taken off everything except the 75mg of Aspirin and the 10 mg of Lipitor. My blood pressure off BP meds. is now typically between 110/70 and 120/80 ish. Doctors have expressed surprise at the recovery made and my current status as being untypical, but only show mild interest when I tell them how I believe it was achieved. I despair sometimes, but keep propounding. Please give some time to studying this most probable cause of CHD and, if you become convinced as I, to promoting knowledge of it.

Hi Liam–

I’m happy that your coronary artery disease has improved, although it was unclear in  your comment whether you had had a bypass, a stent, angioplasty or medical therapy only.  I have spent a fair amount of time studying the vitamin C/heart disease issue.  As of yet, I’m not as convinced as you are of its efficacy.

Cheers–

MRE 

Has anyone heard of Sir Harry Himsworth, who was the first to show a strong link between sat fats and diabetes, way back in 1936? The huge historic rise in sat and trans-fat intake in industrial nations was noted by an astute Oxford biochemist, Dr Hugh Sinclair, who was aware of Himsworth’s findings, and who left the world a simple formula that explains chronic disease in the West.

In his landmark letter to The Lancet in 1956, Sinclair proposed that a high dietary ratio of [Sat + Trans] to Essential Fatty Acids (EFA) might cause a vital deficiency of EFA in cell membranes throughout the body, including mitochondrial membranes.

His ratio, also known the other way around, as the Poly/Sat, or P/S ratio, is rather clever, because it explains how fatty diet can oxidize LDL (without raising total LDL very much), and also oxidize the Good Guy HDL, rendering the latter dysfunctional and dangerous, as well as more abundant!

What causes this crucial oxidation in vascular disease? Sinclair’s mitochondrial membranes, rendered EFA-deficient by fatty diet, are the most likely source of this oxidation, because EFA deficiency causes respiratory uncoupling in mitochondria–a potent source of superoxide free radicals and hydrogen peroxide, which easily oxidize lipoproteins, and also promote vascular inflammation.

Those who (quite rightly) question the importance of dietary fat in heart disease must remind themselves that fat intake, especially from between-meal and late-night snacks, is seriously underestimated by most “Free Range Liars”!

Animal experiments show quite clearly that fatty diet causes insulin resistance, reduced membrane unsaturation, raised glucose and insulin, increased triglycerides and blood pressure, obesity and inflammation.

Sinclair’s cell membrane hypothesis, when applied to pregnancy, also explains the curious syndrome of chronic anxiety, Metabolic Syndrome and Deadly Lipid Triad, seen in 20-30% of Westerners. Fatty maternal diet (low P/S Ratio) in pregnancy causes gestational diabetes (or subclinical pre-diabetes), which are known causes of shyness (anxiety disorder) in the offspring.

At least half of all Type 2 Diabetics and heart patients have this syndrome, showing as anxiety, visceral obesity, hypertension, glucose intolerance, and Deadly Lipid Triad (low HDL, small dense LDL, raised trigs).

These are the ones who often simply drop dead, from anxiety-induced lethal arrhythmias; if they live and reach hospital, they will be noted as coronary cases whose total cholesterol was normal or only slightly raised–thereby starting a great argument.

It is quite possible that such anxious folks do badly on low-fat, high-carb diets, which may raise their trigs even more. But their anxiety drives them to over-eat sweet fatty foods like chocolate, pastries and cakes, so in practice their hi-carbs are usually hi-fat too.

What these folks need is a quick fix for their anxiety and their binge-eating, which will also cure the Deadly Lipid Triad. One simple molecule will do all this–the simple glucose isomer Inositol, abundant in all seeds, whole grains, nuts and legumes, and also found in citrus and rock melon.

Inositol magically reverses anxiety by inhibiting Serotonin 2A receptors in the brain stress circuits, thereby stopping stress-related over-eating; and it raises HDL, and lowers trigs, by lowering peripheral stress hormone activity (less cortisol and noradrenaline).

The world needs more Psycholipidologists, who will treat calm folks eating fatty diet, with a simple low-fat diet; but who will detect anxious cases (“Were you a shy child?”), and treat their Deadly Lipid Triad, their weight problem and their anxiety–all in one Big Hit–by recommending a low-fat, grain- and legume-rich diet. Problem solved!

I wouldn’t say the problem is solved all that categorically.  In fact I don’t think a low-fat, grain- and legume-rich diet will solve the problem at all.  And I suspect that all the speculation on oxidized LDL is simply another ad hoc hypothesis to somehow salvage the lipid hypothesis. 

I do agree that stress is a major cause of heart disease and should always be considered as a causative force.

Cheers–

MRE 

But seriously… it seems all is clear to those who look for the real truth as in the letters above.
Is there any research coming out of the knowledge that there is little useful benefit of cholesterol levels and CHD, in terms of:
a) what IS increasing CHD in middle aged men in western cultures? and
b) just how bad are polyunsaturated (+/- hydrogenation) fats that have become so integrated into supposed ‘healthy’ living over the past half century or so?

Like your work, btw.

Toby

Hi Toby–

Sorry it’s taken me so long to post this–you got caught up in my spam filter, so I just found your comment today.

First, I don’t really think CHD is increasing.  Deaths from CHD are falling, but CHD is kind of holding its own.

Second, I think polyunsaturated fats of the omega-6 variety are dreadful in the amounts people typically consume today; trans fats are even worse. We don’t need any trans fats (of the commercially prepared variety–some of the naturally occurring ones, CLA, for instance, are actually good for us), but we do need a little omega-6.  Just not anywhere near the amounts we’re getting today.

Cheers–

MRE 

Hi PubMed Diver–

What’s wrong with liberal prescription of statins, eh.  Only that they are raising the cost of health care to us all.  Statins are extremely expensive – about $1300-$1400 per year – and most people who take them have drug cards as part of their insurance.  These increased expenses run all of our insurance rates up.  And the ‘rare’ side effects create more medical expenses that add to the burden.  All this could be justified if it reduced the all cause morbidity and mortality, but it doesn’t.  In only serves to cost us all more money for which we get very, very little in return.

Cheers–

MRE 

Release date is September 18, 2007. I was hoping for something sooner, but better late than never. Here’s the Link to the publisher’s site.

Dave

Hi Dave–

I’ve been involved in an intense email exchange with Gary over this title.  I don’t like it, and I don’t think he particularly does either.  Once you read the book, though, the title makes more sense.  But I still don’t like it.  I could have been so much better.

Best–

MRE 

I’m sure somebody talks about it somewhere, but I couldn’t find it (admittedly, I didn’t look that hard, especially after reading Dr. Ravnskov’s
“The Cholesterol Myths”). After 50 years, you think some progress would have been made on this front; or, you’d think the community at large would have put it together that maybe the hypothesis was wrong in the first place.

It’s going to be very interesting if the research decribed in
this article holds water. I think it would be immensely ironic if low carb made it into the nutritional and legislative mainstream because a direct cause/effect relationship could be established between high carbohydrate intake and increased cholesterol level. Even more irony to be found if it is realized that high cholesterol wasn’t the culprit in the first place, but rather CHD was caused by damage do to high blood sugar.

GO BRONCOS!

Dave

Hi Dave–

I’ve got the Nature paper that the ScienceDaily article discusses, but I haven’t had time to read it in depth.  When I do, I’ll probably post on it if it really has merit.  I never trust journalistic interpretations of scientific papers.

I’m in an interesting situation.  I have my money on San Francisco +10, but I want the Broncos to win.  So, root for a Bronco win and a SF cover.

Happy New Year!

MRE