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Saturday, 22 September 2012

More Cholesterol Madness; Malcolm Kendrick on Viral Hepatitis. Plus, What would Jesus eat?

The following is from an article by Malcolm Kendrick, author of The Great Cholesterol Myth.

And so the latest argument is that nobody in modern society has a normal cholesterol level. 
An article in the Journal of the American College of Cardiologybest sums up this line of thinking. Under the heading 'Why average is not normal', O'Keefe, the lead author, makes the claim that: 'Atherosclerosis is endemic in our population, in part because the average LDL ("bad" cholesterol) level is approximately twice the normal physiologic level.' In short, according to O'Keefe, our cholesterol level should be about 2.5mmol/l, not 5.2mmol/l.
This argument, if true, does neatly demolish the question 'How can people with normal, or low, cholesterol levels be protected against heart disease?'. O'Keefe and others would argue that we all have a high cholesterol level. Everyone is ill, and all shall have statins.
One regularly quoted fact, which superficially seems supportive of O'Keefe's hypothesis, is that peasant farmers in China have very low cholesterol levels and a very low rate of heart disease (although their average cholesterol levels are actually about four, not two-and-a-half).
But when you study the figures with more care, they reveal something else. As usual, those with low cholesterol levels have by far the highest mortality rates. Liver failure and liver cancer are common causes of death. However, there is a simple explanation for this association. Many Chinese peasant farmers have chronic hepatitis, which creates low cholesterol levels, and also leads to liver failure and liver cancer. This is why people with low cholesterol levels die young. 
Does this mean that a low cholesterol level protects against heart disease? No: what the Chinese data tell us is that those with higher cholesterol levels are not chronic hepatitis carriers, so they live longer and have more chance of developing heart disease in old age. On the other hand, those with low cholesterol levels cannot die of heart disease, because they are already dead.
Without chasing too many mad arguments around, the simple fact is that everyone in the West does not have a raised cholesterol level. Repeated studies have shown that a perfectly normal, or healthy, cholesterol level lies between about four and six, and lowering it cannot protect against heart disease, otherwise we will have introduced a new concept into medical science: normal is unhealthy and must be treated.


Message; cholesterol that is normal or "high" (the old "normal") is a good thing if you have chronic viral hepatitis. And cholesterol in your diet will provide some of the protection you're lacking if serum cholesterol is low; but it probably won't elevate serum cholesterol. This is more likely with saturated fat in the diet. Polyunsaturated oils and spreads are likely to depress it further.
Dr. Robert Atkins noted (in "Dr Atkin's New Diet Revolution") that his diet - high in fat, very low in carbohydrate - tended to lower cholesterol in patients when it was very high (the "normal" range was more realistic in his day) and raise cholesterol towards the normal range when it was unusually low.

What to eat? Although I revere Dr Atkins, the diets in his books use far too much oil and processed food.
These are two versions of what I think is just about ideal.
by Dr Kurt Harris, and
by Paul and Shou-Ching Jaminet.
I recommend trying the lower end of carbohydrate consumption in either diet; but I also think it's OK to experiment with both higher carb and ketogenic dieting to find out what's ideal for you.The supplements/ special nutrient suggestions in the Perfect Health Diet are valuable too, and if you want recipes The Perfect Health diet blog provides many examples.
Niether diet mentions Hep  C, but that's OK; we're not metabolic freaks, and in this case what's good for so many other people out there with type 2 diabetes, fatty liver, autoimmune problems, and malnutrition seems to be made for us.

In terms of a fasting lipid profile, there are some variables that may matter with regard to Hep C; you want TG (fasting tryglycerides) to be low (lower than HDL, or much the same, is perfect), and you do not want LDL or total cholesterol to be low.
High TG means that more HCV virions can leave the infected cells (estimated to average 50 per cell per day), low LDL means that they have more chance of getting into uninfected cells (because there are more receptors). Lower TG with any given LDL count means that the LDL particles are larger and there are fewer of them, which also reduces HCV virion opportunity. Low LDL may to some extent be compensated by a cholesterol-rich diet, which also reduces LDL receptor numbers.

"in experimental animals such as the hamster and the rabbit, dietary cholesterol increases liver cellular cholesterol and suppresses both hepatic cholesterol synthesis and LDL-receptor expression. In the rat, dietary cholesterol also increases liver cellular cholesterol, but its effect on the LDL-receptor is variable and species-dependent."

referenced in "Dietary Fats and Alcoholic Liver Disease" by Esteban Mezey:


john said...

Hi George,

You made a comment on Hyperlipid about a possible increased need for AA and DHA when eating high fat. What is your argument for this?

I go back and forth, of course hoping to conclude that your suggestion is correct, as it would be nice to the worry about eggs, duck, goose, pork, etc.

George Henderson said...

Of course, if you are eating high fat, you are probably already getting more AA and DHA...
It seems to be the case that an extreme of macronutrient intake sometimes alters the fate of the sub-macronutrients (to coin a phrase), the individual fats, sugars and amino acids. For example, the fate of fructose is less problematic, and AA is preserved, when carbs are low.
Fats affect blood lipids, but so do carbs; in VLC, does the optimal lipid ratio change to reflect this?
For example, very high LDL on a VLC diet (if it means anything, i.e. if it is associated with some other symptom) could obviously be moderated by a higher intake of very long chain fatty acids.
And it appears that hepatic gluconeogenesis in mice is decreased by supplying VLCFA; and this is more effective if krill oil rather than fish oil is used.
This effect could be useful in some VLC scenarios.
Also, in terms of Hep C, adding DHA, AA, and EPA (in order of efficacy) to infected hepatocytes can produce substantial drops in viral replication (I presume that linoleic and maybe linolenic were already supplied in baseline culture medium, being "essential" nutrients)
The foods you mention are low in iron, which may justify including them as alternate protein sources.
A good omega 6:3 ratio seems to be able to compensate for some effects of higher PUFA intake. So add fish to the list. I cook bacon in dripping, fish with coconut, eggs in butter, use dripping in chicken stuffing, etc, so that VLCFA are preserved in an SFA/MUFA matrix.

Before the advent of seed oils, linoleic acid was about 1% of energy, now it is closer to 8%.
Is arachadonic acid from diet different, physiologically, from AA formed from excess linoleate? Like cholesterol, does it depress its own rate of synthesis? More questions than answers.
Maybe, like a reverse vegetarian with a wartime ration book, the high-O6 white meats can be substituted for nuts and seeds and olive oil.

john said...

That's an interesting study about the downregulated gluconeogenesis. Nephropal used to write about fish oil increasing adiponectin, which as far as I know is a factor there. Vitamin D is often claimed to do the same, but I remember being unable to find any direct evidence for vitamin D supplementation increasing adiponectin or decreasing gluconeogenesis.

When you say that "AA is preserved," do you mean its incorporation into tissue versus its metabolism? I wonder if that itself is something to think about anyway. The AA conversion/synthesis does seem to increase and decrease, at least in rats and mice, which is expected.

Linoleic acid is traditionally low, but as you also said on Hyperlipid in response to blogblog, those diets are maybe "new" as well, where there isn't as much reliance on large game and high amounts of fat. I often see the 4%kcal as PUFA mentioned, but that leaves very little room regarding fat sources [if eating high fat].

George Henderson said...

Arachadonic acid is preserved on VLC in a Volek paper - it is not converted to prostaglandins etc, because of less inflammation/ lower insulin.
Robb Wolf has a post on it:

In evolutionary diets we would have been exposed to AA + DHA in good ratios but LA content would have varied seasonally. When eating animals corn-fed year round things might be different.

George Henderson said...

A really good read on this subject is "The Queen of Fats" by Susan Allport.
It turns out leafy greens are an important source of ALA when the diet contains enough of them (and isn't already full of LA).
this may explain the benefits of eating greens... not the fibre, or even the purported antioxidants, but the omegas.
The colder the growing conditions the more omega 3. Watercress is probably ideal; seaweeds are even better (some have EPA and DHA as well).