Here are Loren's responses to your questions. I see no reason why this
can't lead to another batch of questions for Loren. Don.
Hi Don,
Let me try to answer the questions as best I can:
(1) When switching to the Paleo Diet after being on an ultra-low carb
diet, is it possible to gain temporary weight from eating the "unlimited"
fruit allowed on your plan?
Let me take a round about way of answering this question first by
explaining why almost all of the weight we gain comes from either dietary
fat or dietary carbohydrate.
As I pointed out in Chapter 4 of the Paleo Diet, it is
physiologically impossible to gain weight when lean protein is the only
food consumed because of the body's limited ability to break down protein
and excrete the by-product of protein metabolism (urea). This limit is
called the physiological protein ceiling and varies between 30-40% of the
normal caloric intake in most people, assuming they are consuming their
usual (eucaloric) energy intake. Continued consumption of lean protein at
or above the physiological protein ceiling without added fat or
carbohydrate will elicit symptoms of so-called "rabbit starvation", a
malady eliciting lethargy, diarhea, weight loss, electrolyte imbalances and
eventual death. Hence, all people will lose body weight if limited to
consumption of lean protein.
Lean protein has been shown time and again to be the most
satiating of all 3 macronutrients (protein, fat and carbohydrate). Numerous
clinical trials have shown that people eat fewer calories during a high
protein meal compared to high fat or carbohydrate meals, and they also eat
fewer calories at the meal immediately following a high protein
meal. Finally, lean protein has 2-3 times the thermic effect of either
carbohydrate or fat -- meaning that it elevates metabolism ~5-10% higher
than when either carbohydrate or fat are consumed.
Both carbohydrates and fats can be consumed (theoretically) in
quantities greater than the daily energy expended because there is no
physiological limit or ceiling that occurs when these substrates are
metabolized. Excess dietary carbohydrate or excess fat do not make us
acutely ill like excess protein. Hence, these excess calories are simply
stored as body fat. Over the long haul, when more energy is consumed than
energy expended, we gain weight.
Carbohydrates that cause us to gain weight are typically
carbohydrates with a high glycemic load. Although most of you have
probably heard of the glycemic index (the ability of a food to acutely
raise the blood sugar), many are unfamiliar with the glycemic load, which
is simply the glycemic index of a food multiplied by the carbohydrate
content in a given amount of the food. The glycemic load of a food is more
closely related to the net insulin response over a 24 hr period than is the
simple glycemic index. Consequently, it is the glycemic load that may
predispose us to obesity and chronic disease.
Although watermelon has a high glycemic index (72) similar to
white bread (70), it has a glycemic load (per 10 grams of watermelon) that
is only 5.2 compared to a glycemic load in white bread of 34.7. The
International Table of Glycemic Indices lists the glycemic index of 11
fruits. The glycemic loads (per 10 grams of food) of these 11 fruits are
as follows: (bananas 12.1, pineapple 8.2, grapes 7.7, kiwi fruit 7.4, apple
6.0, pear 5.4, watermelon 5.2, orange 5.1, cherries 3.7, peach 3.1,
grapefruit 1.9). Consequently one would have to eat 6.7 times as much
watermelon as white bread to achieve an equivalent glycemic load. Let's
say you ate 4 slices of white bread (or 100 grams ~ 1/4 lb). In order to
get an equivalent glycemic load, you would have to eat almost 1.5 lbs of
watermelon or 4 lbs of grapefruit.
One of the body's mechanisms used to determine when to stop eating
is stomach volume or fullness. Most people would stop eating watermelon
after about 3.0 lbs (435 kcal) or say even 6.0 lbs (870 kcal) because their
stomach volumes simply couldnt physically take much more food. Hence under
normal eating conditions, it is difficult or impossible for most people to
overeat on fruits alone.
However, this being said there are some important
exceptions. Dried fruits are not only concentrated calorie sources, they
also represent high glycemic loads and have a high potential to cause
weight gain, particularly when eaten in unlimited quantities. Also, high
fat foods such as nuts, seeds or fatty meats if consumed in excessive
quantity along with fruits can also promote weight gain.
When I say unlimited quantitites, perhaps I should say, within
normal eating limits, rather than complete gluttony. If you are unsure of
"normal limits" and do not know if you are hungry, then eat a piece of lean
turkey breast. If you are still hungry eat more lean protein, particularly
if weight loss is a major objective.
(2) Is your plan suitable for someone with a hypothyroid condition?
It depends upon the nature of the problem underlying the
hypothyroid condition. If hypothyroidism stems from a tumor or specific
metabolic disorder, then diet will be of little consequence. If the
hypothyroidism stems from general ill health and is of an unknown etiology,
then there is considerable evidence to suggest that the diet I have
outlined may be therapeutic. Hypothyroidism has been frequently observed
in type 2 diabetics and may result partially from the endocrine changes
that result from insulin resistance. Additionally, in animal models, low
dietary protein can elicit low serum thyroxin levels. Further, millet (a
common dietary cereal grain) found in the diet of Africans is known to be
the underlying cause of endemic goiter in these people. Also,
hypothyroidism occurs frequently in celiac patients suggesting that there
may be an immune interaction with the gliadin fraction of wheat and the
thryroid gland. Finally, a diet that produces a net metabolic acidosis
(ala the standard grain, cheese and salt laden western diet) has also been
associated with mild primary hypothyroidism and hyperglucocorticoidism.
Taken together this information suggests that a diet that is high
in protein, of a low glycemic load, contains no cereal grains and produces
a net alkaline load to the kidney may be of therapeutic value. Guess what
-- these nutritional characteristics describe the Paleo Diet to a T!
(3) What is your response to researchers such as Enig and Peat who claim
that coconut oil and dairy products, both full of saturated fat, actually
boost metabolism?
Virtually all metabolic chamber studies examining the ability of
the 3 macronutrients (protein, carbohydrate, fat) to boost metabolism are
in agreement that protein has 2.5 to 3.0 times the thermic effect (ability
to boost metabolism) of either fat or carbohydrate. I am unaware of any
evidence contrary to these established facts.
(4) The Paleo Diet briefly recommends just a very few supplements, but
does not mention any of the "anti-aging" hormonal supplementation that is
so in vogue now such as 7-Keto DHEA, testosterone, pregnenalone, etc.
What effect, if any, does the Paleo Diet have on hormones??
I have addressed how the Paleo Diet influences a variety of
hormonal cascades in Chapter 5 in my book, particularly as it relates to
insulin resistance. The Paleo Diet tends to normalize insulin metabolism
in most people because of its low glycemic carbohydrates, its high protein
content and its beneficial balance of omega 6 and omega 3 fatty acids. The
normalization in insulin influences other hormonal pathways such as the
IGF-1/IGFBP-3 and retinoic acid axis which in turn reduce the risk of many
maladies associated with abnormal or unregulated tissue growth, as
described in my book. Additionally, the high dietary levels on omega 3
fatty acids tend to produce a localized hormone (eiconsanoids) profile that
is anti-inflammatory.
(5) Do you have any thoughts on whether long-term use of a traditional
ultra-low carb diet can interfere with thyroid function?
I'd be strictly speculating here because I believe there is no
direct clinical evidence. However, one of the major problems of the
ultra-low carb diets are that they yield a net metabolic acidosis because
there is insufficient alkaline base (only derived from fruits & veggies) to
neutralize the net renal acid load that the kidney must deal with from a
high meat diet. As I have pointed out in question 2, there is some
evidence that a net metabolic acidosis may elicit a mild primary
hypothyroidism and hyperglucocorticoidism.
(6) Trimming fat from meats is somewhat mandatory in your regime. But there
is nary a mention of whether the fat from grassfed and/or wild game is
exempt from this trimming. What are your thoughts?
We have recently analyzed and compared the fatty acid composition
of wild animals, grass fed beef, and grain fed beef (Cordain L et al. Eur J
Clin Nutr 2002;56:181-91) and have found that the relative saturated fat
content within subcutaneous fat (be it from grain fed cows, grass fed cows,
or wild game) is virtually identical among the three different
animals. However, the absolute amount of saturated fat is 2-3 times higher
in the meat (muscle) of grain fed cows. Consequently, if you would like to
reduce your intake of saturated fat (which I believe to be a prudent
dietary measure), then excess fat should also be trimmed from grass fed
beef meat (muscle). The healthful long chain (>20 carbon) omega 3 fatty
acids are found almost exclusively within the phospholipid fraction of the
muscle membrane.
(7) You recommend canola oil in your book which is surprising considering the
fact that canola has no history in our evolutionary past. I know the
fatty acid profile for this oil is very good but I'm concerned that it
has not been availabe for human consumption until very recently. My take
on this food has always been proceed with caution and I'd like to know
your reasons (aside from the fatty acid profile) for recommending it.
On pages 127-129 of my book, I outline the differences in the
fatty acid composition of the various cooking and salad oils that are
available to consumers. I recommend canola oil because it is high in
monounsaturated fats (58.9%), low in saturated fats (11.6%) and has an
omega 6/omega 3 ration (2.0) that mimics the ratio found in
pre-agricultural diets. These fatty acid characteristics have been shown
in numerous clinical trials to reduce the risk of atherosclerosis and heart
disease, currently the number 1 cause of death in the U.S.
Canola oil comes from the seeds of the rape plant (Brassical rapa
or Brassica campestris) which is a close relative of broccoli, cabage,
brussel sprouts and Kale. Humans have eaten cabbage and its relatives
since prior to historical times. In its original form, rape plants
produced a seed oil than contained high levels (20-50%) of a
monounsaturated fat called erucic acid (22:1n9) that was shown to cause a a
wide variety of pathological changes in laboratory animals. In the early
1970's plant breeders from Canada developed a strain of rape plant that
produced a seed with less than 2% erucic acid (hence the name Canola
oil). The erucic acid content of commercially available canola oil
averages 0.6%. Numerous animal experiments show that the previous health
effects identified with high concentration of erucic acid do not occur at
this concentration, and in fact canola oil prevents potentially fatal heart
arrthymias in animal models. There is no credible scientific evidence
showing that canola oil is harmful to humans.
(8) In his book, Loren lists nuts based on the goodness of their omega
6:omega 3 ratio. He says the ratio should be 2 or 3 to 1. Walnuts are the
best at I think something like 2:1, and he says MAYBE macadamia nuts are
okay at 6:3.
The other nuts go down from there. I'm no math whiz, but isn't 6:3 pretty
much 2:1?
On page 125 & 126 of my book, I list the n6/n3 ratios of commonly
consumed nuts. Walnuts are best with a ratio of 4.2:1, followed by
macadamia nuts with a ratio of 6.3:1. So macadamia nuts have a little
more than 6 times the amount of n6 fatty acids than n3 fatty acids. We
estimate that in Stone Age diets people would have had a net dietary n6 to
n3 ratio of between 2-3:1. Consequently, high consumption of nuts can
swing the n6/n3 balance too high in favor of n6 fatty acids.
(9) I would love to know what the scientific data is on ketosis, and
specifically, if there is any evidence that it is harmful if induced by a
restricted paleo diet.
Most of the scientific data on ketogenic diets concerns the
treatment of refractory epilepsy in children. Ketogenic diets have been
shown to reduce the number of seizures and are routinely prescribed as a
therapeutic modality for this illness. Ketosis is caused by
the metabolism of dietary fat when carbohydrate is unavailable or during
starvation. Ketosis elevates blood levels of two ketone bodies
(D-beta-hydroxybutyrate and acetoacetate) which provide the brain with a
non-glucose substrate, thereby sparing muscle from metabolic destruction
for glucose synthesis -- remember, except for ketones, the brain can only
use glucose as a fuel.
Side effects of ketogenic diets in epileptic children include: 1)
refusal to drink fluids, 2) hypoglycemia, 3) lack of appetite 4) nausea and
vomiting, 5) hypoglycemia 6) elevations of blood cholesterol levels, 7)
constipation 8) anorexia, 9) metabolic acidosis, 10) kidney stones, and 11)
deficiencies of the amino acid carnitine. See Rios G. Rev Neurol
2001;33:909-15.
(10) Why do you recommend using Flax oil in cooking? I thought it should
not be heated.
All oils become partially oxidized when heated and produce
secondary lipid compounds. The amount of oxidation produced is dependent
upon the type of oil, the temperature and the length of
heating. Generally, the fewer number of double bonds (or lesser degree of
saturation), the more stable is the oil to heat. Saturated fats have no
double bonds and are more heat stable than monounsaturated fats (with a
single double bond) which in turn are more stable than polyunsaturated fats
(multiple double bonds. Flaxseed oil contains 20 % monounsaturated fat, 66
% polyunsaturated fat (mainly alpha linolenic acid) and 9.4 % saturated
fat. Studies of ground flaxseed during cooking at temperatures encountered
during baking (350 degrees for 2 hours) show that there is no degradation
of the alpha linolenic acid to oxidized secondary lipid compounds (Flax
Council of Canada). I recommend that flax oil be used under similar
conditions (slow cooking under low heat or brief exposures to moderate heat
such as sauteeing). I do not recommend frying any food with flaxseed oil
under searing or high heat.
(11) I have a question dealing with fatty acids and human brain
development: Many paleodiet researchers (Cordain, Broadhurst,
Cunnane,) think that an increased energy density of food and an
increased supply with DHA (fish, brain) was necessary for human
brain development. This idea will also be discussed in the
forthcomming 71st annual meeting of the American Association of
Physical Anthropologists (see
http://www.physanth.org/annmeet/aapa2002/ajpa2002.pdf : abstracts
from Cordain: p. 57; Broadhurst p. 49). On the other hand vegans
have a normal brain development without any DHA from animal
resources. My question: Can a factor that is not necessary in
ontogenesis really be a necessary factor for phylogenesis?
Numerous studies of vegan vegetarian mothers show that DHA is
reduced in both the tissues of mother and newborn infant and that reduced
plasma concentrations of DHA is associated with both behavioral, cognitive
and visual problems in the developing child/infant when the child/infant is
deprived of preformed DHA. Hence DHA is indeed necessary during ontogenesis.
Also, remember that the brain continues to grow in all primates
long after the weaning period -- more so than in any other altricial
mammal. Hence, additional DHA in the diet (via increased animal food
ingestion) allows for the increased accretion of DHA in the brain over
time. In precocious mammals brain and body growth occurs rapidly,
consequently even if exogenous DHA is available there is little or no time
for accretion.
(12) To what extent is The Paleo Diet based on analyses of the food
sources based on the human fecal remains at paleolithic sites? Some time
ago I read that an analysis of these materials showed that a very large
proportion of the paleolithic diet came from the gathering side
(vegetable sources and perhaps insects or fish) rather than the hunting
side. The Paleo Diet doesn't refer directly to this research, which seems
the most direct approach to knowing what paleolithic humans ate. Rather,
the book seems emphasize hunting as a predominant dietary source.
Coprolites are fossilized fecal remains & except for bones &
feathers do not contain any digestive remnants of animal flesh and
organs. Consequently, coprolites almost universally can only reveal the
plant food types in the diet and cannot quantitatively show the relative
amounts of plant and animal food proportions. Stable isotope studies of
the collagen in Stone Age humans (living in England 13,000 years ago) show
that their diet (in terms of protein content and quality) was
indistinguishable from top level trophic carnivores such as foxes and
wolves.
(13) To what extent to you think the level of small-dense LDL
cholesterol explains the "badness" of LDL? This is relevant to
the paleo diet because small-dense LDL is strongly correlated
with triglycerides. On some conceptions of paleo diet, a more
Atkins-like approach is taken: liberal saturated fat, very low
carb. The result is often somewhat elevated LDL, but very low
triglycerides. The low triglycerides probably indicate low
levels of small-dense particles in the LDL fraction. This is why
the Eades are not concerned about increases in LDL on their plan
(for example). What is your take on this?
Excellent point. We need more information to determine if very
low carbohydrate, high fat diets reduce small dense LDL in all people or
only in certain genetically predisposed people ala the multiple studies
done by Dreon et al. Further it will be necessary to determine whether or
not the total increase in LDL (even with a concomitant decrease in small
dense LDL) still accelerates the atherosclerotic process. It seems most
likely that small dense LDL are derived from triacylglycerols carried in
the VLDL fraction, hence the possilbility looms that a major determinant of
atherosclerosis is the ratio of total LDL/small dense LDL. To my mind, the
evidence points to the notion that atherosclerosis results from many
environmental factors including those dietary elements that simultaneously
raise LDL (high saturated fat diets) and TG (high glycemic load
diets). Both of these dietary characteristics could not have been part of
any Paleolithic Diet.
Thank you all for some very, very good questions!
Cordially,
Loren
Loren Cordain, Ph.D., Professor
Department of Health and Exercise Science
Colorado State University
Fort Collins, CO 80523
tel: (970) 491-7436
fax: (970) 491-0445
email:[log in to unmask]
http://www.cahs.colostate.edu/hes/cordain.htm
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