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Subject:
From:
Todd Moody <[log in to unmask]>
Reply To:
Paleolithic Eating Support List <[log in to unmask]>
Date:
Fri, 26 Jan 2007 09:41:24 -0500
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Philip wrote:
> I'm puzzled by Sears, the Eades and Artemis Simopoulos citing paleolithic
> nutrition as the justification for their diets and then going ahead and
> recommending some non-Paleo foods as a regular part of the diet anyway. I
> read the first couple chapters of Simopoulos' _The Omega Diet_ and skimmed
> the rest. It was bizarre to read her agreeing completely with Eaton and
> Cordain in the first chapter and then in the following chapters recommending
> the very foods she had so convincingly weighed against. How she reconciles
> bagels with Paleolithic nutrition I cannot imagine.
>   

In the case of Sears, I think it's a matter of deciding that paleolithic 
nutrition provided some confirmation for conclusions that he had reached 
in other ways.  I feel a certain debt of gratitude to Sears because it 
was reading his book that put me onto the idea that carbs, rather than 
fat, could be problematic.  Atkins had been around for a long time, as 
well as other lowcarb pioneers, but I knew little or nothing of them and 
was generally as brainwashed as everyone else.  Sears was also the 
first, to my knowledge, to highlight the important interactions between 
carbs, insulin, and the prostaglandins (eicosanoids) in a popular 
format, and the pro-inflammatory nature of a high-carb diet.

> OK, if I've understand correctly now, you started NeanderThin after the most
> recent test results you shared, so those stats are irrelevant to your
> experience on the NeanderThin diet, correct, and the problems you
> experienced (such as huge increase in LDL after about 6 months) can be
> attributed to Zone rather than NeanderThin? If so, why did you stop doing
> NeanderThin?
>   
No.  I started Neanderthin *between* the Jan. and June 1997 blood 
tests.  Roughly, it was Zone from Jan. to mid-March, and Neanderthin 
from late March to June (and beyond).  So the huge increase in LDL 
occurred after roughly three months of each.  And of course my diet 
before Jan. 1997 was SAD.  Frankly, I doubt very much that the Zone, 
which is quite calorically and SFA restricted, sent my LDL up.

Why did I eventually stop Neanderthin?  I don't really remember.  I'm a 
ceaseless tinkerer, and so it was (and is) natural for me to 
experiment.  I wasn't losing weight on Neanderthin, and I had doubts 
about some of the ideas in the book, such as the foreign protein, 
autoimmune stuff.

> The studies are stronger on small-dense-LDL, that's for sure, but I think
> the starting point is opposite of where it should be. Instead of scientists
> starting with what they rather arbitrarily think is a "normal" range for LDL
> based on data from Americans on the SAD and then demanding evidence of why
> HG LDL should be deemed optimal (while gradually lowering the top of the
> range from 130 to 120 to 100 as studies demonstrate benefits from lower
> levels of LDL), they should start with the H-G data showing LDL 30-70 as the
> "optimal" range and require evidence that higher levels of LDL are
> healthier. I think the burden of proof lies with those who think LDL above
> 70 is OK.
Healthier, or just OK?

It seems to me the question is whether elevated LDL, in itself, plays a 
causative role in any disease process.  As you know, correlation doesn't 
imply causation.  Suppose elevated LDL is in itself harmless but can be 
caused by two things, A and B.  Suppose A is a process that also causes 
cardiovascular disease, but B doesn't cause any disease.  And suppose in 
any given population, there is a mix of A-caused and B-caused elevated 
LDL.  In those populations, there will be some (variable) degree of 
correlation between elevated LDL and cardiovascular disease, because 
elevated LDL will be a marker (imperfect, but significant) for process 
A.  But if LDL itself plays no causative role, then it's really process 
A that should be addressed.  I think something like this is in fact what 
we have in reality.

>> I think that
>> increased SFA
>> intake causes a temporary LDL increase in many people, 
>> although in those 
>> who are also losing weight at a good clip it may not be so.  
>> Fortunately, we now have (but didn't in 1997) some excellent 
>> controlled 
>> studies of VLC (very low carb) diets that are high in SFA, and the 
>> evidence from those studies is reassuring.  See for example 
>> http://www.obesityresearch.org/cgi/content/full/12/suppl_2/115S
>>     
>
> Interesting, though the studies showed a return to baseline LDL after 6-8
> weeks in subjects with minimal weight loss and a small drop in LDL for most
> subjects with weight loss, whereas you experienced a huge increase in LDL
> after over 20 weeks. Since you were apparently on a Zone diet (30% carbs)
> instead of a VLCKD (6-10% carbs), this may account for your LDL increase.
>   
At the time of the test, I had been on Neanderthin for 12 weeks or so, 
and had regained a bit of weight.  Some but not all of that would have 
been muscle, because it's pretty clear that I was losing muscle on the Zone.

> What I mean is, since you said that few people can lose dramatic amounts of
> weight on a Paleo diet while following the "eat until you're full" rule,
> then few Westerners are going to experience dramatic weight loss and blood
> sugar improvements without doing IF or caloric restriction, right?
>   
I have no idea whether it's few or many who fall into this category, but 
it's clear that at least some do.


> I agree that damage done by modern foods makes it more difficult to match HG
> health characteristics and some types of damage cannot be undone completely.
> Another example that supports what you're saying is that some HG tribes
> appear to be able to gorge on honey while it's in season without any
> apparent IR problems and honey has been found to be generally benign--even
> healthy--in some studies, whereas someone who already has IR or diabetes
> would probably not be able to consume honey without spiking their BS badly
> and likely doing some damage.
>   
That's how I see it.  I'm sure that HGs could handle starches in the 
form of foraged tubers and rhizomes with no problem, but for someone 
whose system is burnt out from years of eating pasta, it's a different 
story.

> 1-2 meals per day does seem close to your intermittent fasting experiment,
> though HG's don't do the calorie restriction that you're doing (I found the
> following, which indicates that shortage of food was not generally a problem
> for H-G's, and matches the observations of the !Kung San in the harsh
> Kalahari desert: Cordain L, Miller J, Mann N. Scant evidence of periodic
> starvation among hunter-gatherers. Diabetologia 1999; 42:383-84.)
>   

I'm not making a conscious effort to restrict calories, and my rate of 
weight loss at the moment is fairly slow.


> I agree with Audette that saturated fat doesn't appear to be as bad as it's
> usually portrayed, but it also doesn't make sense that eating farmed cattle
> meat that has been bred for centuries to be fatter and that is fed a diet
> that makes it still fatter while kept penned up in a feed lot and requires
> giving it antibiotics to keep it from getting very sick would be just as
> healthy as eating bison meat from a free-range animal that has not been bred
> to be fatter, has been fed less or no grain, and doesn't require antibiotics
> to survive. It seems to me that the flesh of a sick animal on drugs would
> not be as healthy as the flesh of a healthy animal. Even if the saturated
> fat warnings turn out to be completely bogus, wild and pasture-fed animal
> flesh has a healthier profile in other respects as well--such as higher
> levels of omega 3 FA's. Ray Audette's claims that fattening animals makes
> sense because it gives them the higher levels of fatty tissue that ice-age
> large game had doesn't address the issue of the drop in omega 3's and other
> changes in the health profile of these farmed animals.
>   

Inland hominids without a lot of access to cold-water marine fats would 
have gotten their omega 3 fats from brains, I think.  Animal brains are 
omega 3 aggregators, so the amounts and ratios of omega 3s in various 
muscle meats is, in my view, a red herring.  Much of the "drop" in omega 
3 in feedlot meat is an artifact of the increase in overall fat; the 
absolute amounts aren't so different, i.e., minuscule.  But those of us 
who don't eat brains must either eat fatty fish or supplement with fish 
oil.  The meat of land animals just isn't a good source.

In the U.S., cattle (for beef) are weaned at six months, pastured for 
six to eight months, and then fattened in feedlots for three to four 
months.  Thus, they are slaughtered at between 16-18 months, typically.  
The antiobiotics are used in subtherapeutic doses as a kind of 
prophylaxis, so that an infection that one animal might contract doesn't 
wipe out the lot, and also because they promote fattening.  It's not 
because the cattle are generally sick.  What's most problematic about 
this practice is that it breeds antibiotic-resistant microorganisms.

Todd Moody
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