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The Effects of Diet on Testosterone Part 1 & 2
Calories and Protein
by Thomas Incledon and Lori Gross
Introduction
This article will be divided into two parts. Part
1 presents an overview of how testosterone is
stimulated in the body, shows how calorie balance
affects T production, and discusses how dietary
protein intake affects circulating T levels. Part
2 explains how carbohydrates and fats impact
testosterone synthesis and circulation, and then
puts it all together for you to make informed
decisions. Keep in mind that this is a very
complicated and dynamic process. References will
be limited primarily to studies on men. However,
animal research will be cited when it becomes
necessary to discuss proposed mechanisms, or how
the actual changes in the body take place. While
the information may get technical at times, read
on because you will learn a great deal that you
may wish to apply to your own diet.
The HPT Axis
An article on the effects of diet on hormones
would be incomplete without a basic overview of
the relationships between the organs and hormones
of the axis. The term axis simply refers to the
pathway in question. The glands of this pathway
include the hypothalamus, pituitary, and testes.
The sequence of events culminating with the
production and/or release of T begins at the
hypothalamus. Here specialized nerve cells release
a hormone called gonadotropin-releasing hormone
(GnRH). GnRH is a decapeptide (chain of ten amino
acids) that travels by direct blood vessel
connections to the anterior pituitary where it
stimulates the release of luteinizing hormone (LH)
(1). LH is then secreted into the blood where it
attaches to receptors on the Leydig cells of the
testes. This induces activity of an enzyme,
P-450scc, referred to as the
cholesterol-side-chain-cleavage enzyme (1).
Through a series of five enzymatic steps,
cholesterol is converted into T.
The body regulates the circulating blood levels of
T via several mechanisms. Once in the blood, about
44% of T is bound to a protein called either
sex-hormone-binding-globulin (SHBG) or
testosterone-binding globulin (TeBG), to indicate
the greater affinity for T over estradiol (E2, an
estrogen). About 54% of T is bound by albumin and
other proteins, leaving 2% to circulate unbound to
any protein. This unbound T is termed free
testosterone (fT) (1). It is currently believed
that only the fT or albumin bound T are truly
available to interact with the tissues of the
body. The significance of this point will be
elaborated upon later in reviews of the data from
different studies. Of the T that is available to
interact with tissues, some of it binds to steroid
receptors. In most tissues, like skeletal muscle,
it will directly stimulate protein synthesis. In
some tissues, like the brain and fat cells, it can
be converted into E2 via the aromatase enzyme. In
other tissues, like the prostate gland, it can be
converted into dihydrotestosterone (DHT) via the
5-alpha-reductase enzyme. T either directly or
through conversion to E2 or DHT can inhibit its
own future production. The conversion to E2 or DHT
can take place both in the brain and various other
tissues. E2 and T exert stronger inhibitory
effects than DHT on T production. This process is
called negative-feedback inhibition. This is the
reason why the use of steroids, enzyme inhibitors,
and prohormones are far from perfect in their
effects on increasing T levels. Because it is a
dynamic process, as T levels elevate in the blood,
a corresponding increase in inhibitory signals
occurs. This results in the body making less T.
The opposite occurs when T levels decrease. This
is a basic overview and presented in a simplistic
static fashion. The body is a highly dynamic
organism and many factors come into play to help
regulate this process. This point is made to
illustrate the confounding problem that occurs
when trying to increase circulating levels of
androgens.
Effects of Calorie Intake on Testosterone
Every minute of the day, someone makes a decision
to lose weight. Dieting by means of restricting
calories, while not always successful, is
practiced frequently. There are some people who
believe that fasting (or what we call planned
starvation) is a necessary method for cleaning the
body of wastes. What effects does depriving the
body of calories have on endocrine responses
within the HPT axis? As you may have already
guessed, it screws things up. Fasting for 5 days
can lower LH, T, and fT by 30-50% (2). What
appears to happen is that as the body becomes
deprived of energy, less GnRH is released from the
hypothalamus. This, in turn, leads to a weaker
signal to release LH. While the pattern of LH
release remains the same, the amount of LH
released at each interval decreases, meaning your
body is giving weaker signals to stimulate T. In
addition, research on fasting in rats indicates
that testicular enzymes involved in synthesizing T
decrease in function (3). This means that even if
enough LH reaches the testes, they still cannot
produce normal amounts of T. The decrease in T can
be a contributing factor to the loss in lean body
mass that occurs with fasting. Of course, this is
contrary to what most of us want to do in the
quest to get bigger and stronger. However, many
elite athletes have learned how to apply fasting
to their contest preparation. Fasting before a
drug test is a common practice when on
anabolic-androgenic steroids because it helps
prevent testing positive. But before you run out
and load up on some "juice" and think you’ll beat
a drug test just by fasting, keep in mind that
this method is not always reliable, nor does it
work when you have foreign metabolites in the
body.
One of the common problems when dieting is holding
onto all that hard earned muscle. Severe calorie
restriction, whether from reduced food intake or
imposed by excessive exercise, lowers testosterone
(4). While there are no numbers written in stone,
a decrease in calories by 15% does not lower T
levels (5). This may serve as one factor to
consider when planning out a diet strategy. If you
cut back too much on your calories, then you risk
lowering your T, which can cause you to say
goodbye to some of your muscle. The good news is
that when refeeding resumes and calorie intake
equals calorie expenditure, in most cases, T
levels will rise back to normal. The bad news is
that if you are engaging in chronic high volume
endurance exercise, even extra calories won’t help
raise your T levels back to normal.
When male subjects are overfed in an attempt to
induce weight gain, there tends to be a decrease
in T levels as upper body fat increases (6). It
may be wise, therefore, to limit calorie intakes
to less than 1000 Calories (kilocalories) above
energy requirements. From reviewing the
literature, it seems that with large short-term
increases in body fat and small chronic increases,
T levels go down. Perhaps this is due to an
inverse relationship between T and insulin and/or
the aromatase enzyme. It is clear that with
excessive body fat, aromatase activity in fat
cells increases, thus more of T is converted into
an estrogen called estradiol (E2). The issue with
insulin is far more complicated and not really
clear. Some research has shown insulin to regulate
T in a positive fashion (7), while carbohydrate
and protein liquid meals, which elevate insulin,
have been shown to decrease T in resistance-
trained males (8,9). This may be due to an
increased uptake by tissues, like skeletal muscle,
increased excretion of T in the urine, or
decreased responsiveness of the testes to produce
T.
While not related to caloric intake, hydration and
sleep status are also important. A reduction of
3.8% in body weight due to dehydration did not
affect T levels during mild exercise (10). But,
don’t take any chances with hydration. Drink
plenty of water every day at the rate of 30 cc per
kilogram of body weight (or roughly one ounce for
every two pounds). Get plenty of sleep, as
disturbances in sleep and light/dark cycles can
decrease T by almost 50% (11). Of course, no one
ever gets enough sleep!
Dietary Protein Intake & Testosterone
The direct impact of protein by itself on T levels
has not been well studied in humans. Some research
on high protein diets deals with the effects on
very obese people and weight loss. While this may
not seem applicable to you, read on and we will
put it together for you. In obese men, feeding 600
calories a day with 400 calories from protein (50
grams of beef protein and 50 grams of casein)
induces lower levels of T than fasting does (12).
Normally, when the kidneys filter T out of the
blood, some T gets reabsorbed back out of the
kidneys into the blood. The researchers stated
that the additional protein in the diet generated
more ketones. They concluded that the ketones were
filtered out of the blood by the kidneys and were
reabsorbed back into circulation preferentially
over T. While most people reading this may not be
obese, higher protein diets are definitely in
vogue, more so for bodybuilders and powerlifters
than other groups of athletes. The potential
exists that if a ketogenic diet like the Atkins
Diet or a cyclical ketogenic diet like the
Anabolic Diet or Bodyopus is followed, than
urinary excretion of T will be greater during the
ketogenic phase of the diet.
It is known that protein in the diet can influence
the metabolism of a variety of chemicals. Through
a series of experiments, it was demonstrated that
various foods could influence the metabolism of
drugs in the body (13). Vegetables like cabbage
and brussel sprouts were found to alter the
function of specific liver enzymes. This, in turn,
could change the half-life of a drug in the blood.
Given the variety of diets that people follow and
the variety of prescription medications and
over-the-counter drugs people take, the logical
progression was to look at how altering the
macronutrient composition of the diet affected
drug metabolism. It turns out that a higher ratio
protein diet, a diet with more calories from
protein than carbohydrates or fat, metabolizes
some drugs faster, thus decreasing the clearance
time of the drug. Since diet can affect drug
metabolism, perhaps it could affect liver enzymes
involved in the metabolism of endogenous steroids.
Sure enough, it was found that a high ratio
protein diet decreased the reduction of T (14).
Reducing the reduction of T could mean a potential
decrease in DHT and/or androsterone in the blood,
which is good by most accounts. However, DHT
levels were not measured and, more importantly,
urinary T excretion increased, although it was not
statistically significant. These subjects were not
in ketosis, so perhaps ketones do not increase T
excretion rates. Regardless of the exact
mechanism, there is sufficient evidence in the
literature that when protein intake exceeds
carbohydrate intake, T clearance increases by
excretion in the urine.
A cross over design study used seven normal men
from 23-43 years of age and compared a high
protein diet to a high carbohydrate diet (15).
This study has been referenced many times and
cited as proof that high protein diets lower total
T levels in the blood. The high carbohydrate diet
from this study will be covered in Part II. The
high protein diet consisted of 44% protein, 35%
carbohydrate, and 21% fat and supplied between
2400 and 2500 kilocalories per day (kcals/d).
Let’s assume it was an even 2450 kcals/d. The men
also had bodyweights that ranged from 64-72 kg. If
we assume the mean was 68 kg, then this would give
us an average body weight of about 150 pounds.
This means these guys were eating [(2450 kcals/d
times .44) (divide by 4)] 270 grams (g) of
protein, [(2450 x.350 /4] 215 g of carbohydrates
(CHO) and [(2450 x .21) /9] 58 g of fat per day.
However, total T is not that big of a deal. The
more important measure is the bioactive fraction
of T. (Earlier in the overview of the HPT Axis, it
was mentioned that SHBG-bound T is not considered
bioactive, while the other fractions of T are).
While subjects followed the high protein diet,
their total T levels were 28% lower than on the
higher CHO diet (15). This is important because T
decreased in all seven subjects, although the
magnitudes of the decrease ranged from 10 to 93%.
For the same seven subjects, their SHBG levels
decreased about 39% with a range from 19 to 64%.
Looking at this data gives the impression that the
actual bioactivity of T was higher while the
subjects were on a high protein diet. SHBG-bound T
and fT were not measured, so it is not known for
sure. On the surface it appears that a mean
decrease of 39% in the SHBG values and only a 28%
in the T would leave more T available for binding
to tissues. However, if we calculate out the
actual changes in the hormones using the data from
the study, we see something different. The mean
and standard error (M±SE) for T was 371 ± 23
ng/dL. The currently used units in clinical
chemistry are nmol/L. Multiplying the mean T by
the conversion factor of 0.0347 gives us about
12.9 ± .8 nmol/L. The M±SE SHBG was 23.4 ± 1.6
nmol/L. If we assume that the amount of T bound to
SHBG averages 44%, then .44 x 12.9 ± .8 nmol/L
gives us 5.7 ± .4 nmol/L of T bound to SHBG. That
leaves 7.2 ± .4 nmol/L of T to interact with
tissues in the body. However, we don’t know from
the data if the amount of SHBG bound T decreased
below or increased above the normal 44%, in which
case there would be more or less T available to
interact with tissues.
From work by the same group of researchers using
the exact same diet (but different subjects) we
see that the ratio of 5a - reduction to 5b -
reduction (5a /5b ) of T is reduced by about 50%,
with the decrease being attributed to lower rates
of 5a - reduction (14). The T values that have
been used thus far (15) already reflect any
changes in altered T metabolism, so the conversion
to a 5a - reduced hormone (ie androsterone) is
accounted for at this point. Note that even though
there is a decrease in 5a - reduced hormone
production, it does not show up as increased T
levels. The decrease in androsterone probably
shows up in small, but statistically insignificant
increases in other metabolites of T (they were
statistically insignificant perhaps due to the
small sample size). Another interesting aspect is
that there is an increase in the oxidation of
estradiol on the higher protein diet by about
14-15% (14). Unfortunately estradiol levels were
not measured in this paper. This could have given
us clues as to the mechanism by which higher
protein diets lower T (ie increased negative
feedback on T levels via estradiol). At this
point, this is only one study and it is still
difficult to come to any final conclusions.
However, if this is what really happens, then a
high-protein diet may actually lower the anabolic
actions of T in the body. Unfortunately, this has
not been verified through laboratory research and
is just a theory at this point. Perhaps the
decrease in T is a result of increased excretion
in the urine either as T or a sulfated metabolite,
or increased conversion to estradiol and oxidation
by the liver.
Prelude to the Effects of Diet on Testosterone
Part II: Carbohydrates and Fat
We hope so far that you have learned something
about testosterone production and the effects of
calorie intake and protein intake on testosterone
levels in the blood. Please feel free to contact
us if you have any questions or comments at
lorig8r@sprynet.com . In the next article, the
effects of carbohydrates and fat and total T
levels and its components are explained. We will
then review the key points and see how the
information can be integrated into a diet
strategy. At this point we would like to thank
Albert Jenab for his technical assistance and
insight.
References
1) Griffin JE. & Ojeda SR, editors of: Textbook of
Endocrine Physiology, 3rd edition. New York,
Oxford University Press, 1996.
2) Aloi JA. Bergendahl M. Iranmanesh A. Veldhuis
JD. Pulsatile intravenous gonadotropin-releasing
hormone administration averts fasting-induced
hypogonadotropism and hypoandrogenemia in healthy,
normal weight men. Journal of Clinical
Endocrinology & Metabolism. 82(5):1543-8, 1997
May.
3) Fanjul LF. Ruiz de Galarreta CM. Effects of
starvation in rats on serum levels of
testosterone, dihydrotestosterone and testicular 3
beta-hydroxysteroid dehydrogenase activity.
Hormone & Metabolic Research. 13(6):356-8, 1981
Jun.
4) Marniemi J. Vuori I. Kinnunen V. Rahkila P.
Vainikka M. Peltonen P. Metabolic changes induced
by combined prolonged exercise and low-calorie
intake in man. European Journal of Applied
Physiology & Occupational Physiology. 53(2):121-7,
1984.
5) Garrel DR. Todd KS. Pugeat MM. Calloway DH.
Hormonal changes in normal men under marginally
negative energy balance. American Journal of
Clinical Nutrition. 39(6):930-6, 1984 Jun.
6) Pritchard J. Despres JP. Gagnon J. Tchernof A.
Nadeau A. Tremblay A. Bouchard C. Plasma adrenal,
gonadal, and conjugated steroids before and after
long-term overfeeding in identical twins. Journal
of Clinical Endocrinology & Metabolism.
83(9):3277-84, 1998 Sep.
7) Pasquali R. Macor C. Vicennati V. Novo F. De
lasio R. Mesini P. Boschi S. Casimirri F. Vettor
R. Effects of acute hyperinsulinemia on
testosterone serum concentrations in adult obese
and normal-weight men. Metabolism: Clinical &
Experimental. 46(5):526-9, 1997 May.
8) Kraemer WJ. Volek JS. Bush JA. Putukian M.
Sebastianelli WJ. Hormonal responses to
consecutive days of heavy-resistance exercise with
or without nutritional supplementation. Journal of
Applied Physiology. 85(4):1544-55, 1998 Oct.
9) Chandler RM. Byrne HK. Patterson JG. and Ivy
JL. Dietary supplements affect the anabolic
hormones after weight-training exercise. Journal
of Applied Physiology. 76(2): 839-845, 1994 Feb.
10) Hoffman JR. Maresh CM. Armstrong LE. Gabaree
CL. Bergeron MF. Kenefick RW. Castellani JW.
Ahlquist LE. Ward A. Effects of hydration state on
plasma testosterone, cortisol and catecholamine
concentrations before and during mild exercise at
elevated temperature. European Journal of Applied
Physiology & Occupational Physiology.
69(4):294-300, 1994.
11) Cortes-Gallegos V. Sojo Aranda I. Gio Pelaez
RM. Disturbing the light-darkness pattern reduces
circulating testosterone in healthy men. Archives
of Andrology. 40(2):129-32, 1998 Mar-Apr.
12) Hoffer LJ. Beitins IZ. Kyung NH. Bistrian BR.
Effects of severe dietary restriction on male
reproductive hormones. Journal of Clinical
Endocrinology & Metabolism. 62(2):288-92, 1986
Feb.
13) Anderson KE. Conney AH. Kappas A. Nutrition as
an environmental influence on chemical metabolism
in man. Progress in Clinical & Biological
Research. 214:39-54, 1986.
14) Kappas A. Anderson KE. Conney AH. Pantuck EJ.
Fishman J. Bradlow HL. Nutrition-endocrine
interactions: induction of reciprocal changes in
the delta 4-5 alpha-reduction of testosterone and
the cytochrome P-450-dependent oxidation of
estradiol by dietary macronutrients in man.
Proceedings of the National Academy of Sciences of
the United States of America. 80(24):7646-9, 1983
Dec.
15) Anderson KE. Rosner W. Khan MS. New MI. Pang
SY. Wissel PS. Kappas A. Diet-hormone
interactions: protein/carbohydrate ratio alters
reciprocally the plasma levels of testosterone and
cortisol and their respective binding globulins in
man. Life Sciences. 40(18):1761-8, 1987 May 4.
__________________
The Effects of Diet on Testosterone (Part 2):
Carbohydrates and Fats
by Thomas Incledon and Lori Gross
Introduction
Part One of this article explained the impact of
calories and dietary protein (PRO) on endogenous
testosterone (T) levels. As promised, this
continuation will focus on the role of dietary
carbohydrates (CHO) and dietary fat on modulating
T production. The role of CHO on T production is
indirectly addressed when discussing the role of
PRO or fat, so this will be reviewed briefly. The
effects of fat on T are far more complicated and
often time more confusing than the previously
discussed macronutrients. To facilitate an
understanding of the links between dietary fats or
lipids and T, several tables will be presented. An
explanation will accompany each table and key
references will be reviewed. The article ends with
an application of the information to the design of
a dietary strategy to either maximize or minimize
T levels.
Dietary Carbohydrate Intake & Testosterone
Dietary carbohydrates can influence the metabolism
of a variety of chemicals. When fat is held at
approximately 20% of caloric intake, CHO may
elevate T levels (1). Part One of this article
discussed that while this may be true, there is
also a corresponding increase in sex hormone
binding-globulin (SHBG). Anderson et al (1)
compared the effects of a higher PRO diet versus a
higher CHO diet on T levels. Part one discussed
the data on the high protein diet. The higher CHO
diet contained approximately 2450 kcals/d, 70%
CHO, 10% PRO, 20% fat. This provides 429 g/d CHO,
62 g/d PRO, and 55 g/d fat. The seven men in this
study had a range of body weights from 64-72 kg.
If a mean of 68 kg is assumed, then these subjects
were taking in .91g PRO/kg BW or slightly higher
than the RDA of .8g/kg BW. This point is made
because most people take in more protein than this
on a daily basis.
Now let’s get back to the T and SHBG issue. The
interaction between T and SHBG is important to
consider. About 44% of total T is bound to SHBG
and is called SHBG-T. If T increases more than the
SHBG-T fraction does, then the biological actions
of T will be greater because more of it will be
available to bind to muscle and other tissues’
receptors. If T increases less than SHBG-T
fraction, then the biological actions of T will
decrease because less of it will be available to
bind to muscle and other tissues’ receptors.
Anderson et al did not measure SHBG-T. The study
did measure total T and SHBG. It can be seen from
their data, that T increases less than SHBG did on
the higher CHO diet with a ratio of 7:1 (CHO:PRO).
The T values were 16.2 ± 1.2 nmol/L. This was a
28% increase over the high PRO diet and the range
of increases in the subjects was from 10-93%.
Assuming that the SHBG-T fraction remained at 44%
of T, then the amount of T that was bioavailable
would be about 9.1 ± .66 nmol/L. Compared to the
amount of bioavailable T on the high PRO diet,
there is an additional 1.9 ± .21 nmol/L of
bioavailable T.
Also keep in mind that this same type of diet
increases the ability of the liver to reduce T to
5a - reduced hormones (ie androsterone) (2), which
may or may not be something you want (depending on
the study you read). However, this is especially
important for steroid and prohormone users because
a higher CHO diet may increase the conversion of
the exogenous T to androsterone. This is not to
say that diets with higher CHO than PRO will cause
this to occur. What this means is that very high
CHO:PRO ratios like 7:1 or greater may not be the
healthiest way to go, based upon direct and
indirect evidence that androsterone is linked to
acne and prostate disorders.
The effects of CHO on T were just discussed while
fat was kept constant in the diet at about 20% of
calories. When PRO is kept constant in the diet,
higher CHO may actually lower T (8). Hamalainen et
al (8) compared the effects of a dietary
intervention on the hormone levels of 30 men. PRO
intake was fairly consistent while the CHO was
increased from 45% to 56% of calories for six
weeks, and then decreased to 47% for six weeks.
Fat intake was correspondingly decreased from 40%
to 25%, and then increased to 37%. During the
higher CHO period, T and fT decreased
significantly. However, this study was difficult
to interpret because dietary fibers, like pectin
from fruit or bran from wheat, and fatty acids,
like saturated fatty acids or polyunsaturated
fatty acids, can also have an impact on T
production. In the Hamalainen et al study, they
also changed the fatty acid ratios of the diets.
Perhaps the ratio of fatty acids, as opposed to
the amount of CHO or fat, had a larger impact on T
production. Extrapolating this further, maybe it
is not the amount of CHO or the CHO:PRO that
influences T production, but the ratio of CHO to a
particular fatty acid, or some other nutrient
interaction (ie PRO to fatty acid or ratio of
fatty acids).
Correlation Studies Between Dietary Fat Intake and
Testosterone Levels in Men
Fat has received tremendous attention over the
last few years and has been linked to improved
performance and favorable body composition
alterations in the lay journals, despite a lack of
convincing scientific data. The relationship
between dietary lipids and T is important in order
to understand the role that fat may have in
improving performance, altering body fat, or
preventing/initiating disease.
One of the reasons why the scientific data has not
been clear in explaining the role of dietary fat
on T levels is a difference in study designs.
Table 1 displays the data and results from several
studies that compared T, free testosterone (fT),
and/or SHBG levels with total fat or types of
fatty acids in the diet. Data is listed as the
mean values (when available). Correlation studies,
while very common, are far from complete. They
don’t explain if dietary fat or some fraction,
like polyunsaturated fatty acids (PUFA), affects
T, rather they only state if there is a
relationship between one event and another. The
relationship can be positive and an example of
this is reference 19 from Table 1. From the
results column the code FCT is listed in the
results column. FCT means that as the percentage
of calories from fat, grams of saturated fat, and
grams of monounsaturated fat (MUFA) increased in
the diet, there was also a corresponding
association with higher T levels. This study was
done with resistance trained males and is the most
applicable from all of the above studies. The
scope of this article precludes an in-depth
analysis of each study and the associated design
flaws. Most important is to cite the common
findings. From Table 1, several relationships can
be seen. Subjects consuming vegetarian diets have
demonstrated higher SHBG levels (3, 13), lower T
levels (12), and lower levels of available T (3).
One flaw with many of these studies is isolating
the impact of fat on the diet as opposed to fiber,
which is also much higher in vegetarian-type
diets. Another problem with correlational studies
is that they don’t tell you what happens when
subjects are switched from one type of diet to
another. Unfortunately studies sometimes
contradict each other. For example, Bishop et al
(4) examined the role of dietary nutrients on sex
hormone differences between monozygotic twins
(identical twins). The investigators found an
inverse (or negative) relationship between dietary
fats and T. Volek et al (17) however, found a
positive relationship between dietary fat and T.
This further demonstrates the problem of reading
the scientific literature and making sense of all
the information.
Acute Effects of Dietary Fat on Testosterone
A better study design than a correlational study
to determine the effects of manipulating dietary
macronutrients is a randomized cross over,
double-blind study. Cross over means that every
subject experiences all of the different dietary
treatments. By randomizing the order, the effect
of one diet on another is avoided (this is called
order effect). Double-blind means that the
subjects, the people working with the subjects,
and the people tracking the data are all unaware
of the treatment conditions. This is very
difficult to do with feeding studies, so in most
cases a double-blind approach is not used.
Therefore, in most studies, the subjects and/or
the researchers know what the treatment conditions
are. One way the researchers avoid this problem is
to offer milk shakes that taste the same, but, in
fact, have different macronutrient compositions.
While this may be acceptable to study the acute
effects of more or less fat in a meal, this would
not work for chronic studies. After all, could you
drink the same milkshake all day long for weeks
and weeks, or worse yet eat some type of
engineered food product not knowing what was
inside?
Acute studies examine the effects of different
treatments within the hours or days after the
dietary manipulation. In general, the subjects are
given different types of diets and the results of
each diet are compared. This is one way to look at
the effects of a particular nutrient on hormone
levels or blood glucose levels, for example. Table
2 presents the tabulated data from two short term
or acute studies.
In one study (14), the effects of high fat (HF)
and low fat (LF) meals on T levels were compared.
The subjects were given a lemon-lime artificially
sweetened beverage and the hormonal responses
served as a control © for the other meals. A HF
liquid meal containing about 795 calories and made
up of 57% fat (50.4 g fat), 9% protein (17.9 g
PRO), and 34% carbohydrate (67.5 g CHO) was given
on another occasion. The third or final liquid
meal (LF) consisted of 797 calories made up of
1.2% fat (1 g fat), 25.5 % PRO (51 g PRO), and
73.3% CHO (146 g of CHO). The C and LF meals did
not effect luteinizing hormone (LH), T, fT or
dihydrotestosterone (DHT) levels. The HF meal
decreased T and fT up to 4 hours post ingestion
compared to the other liquid meals without
affecting any of the other hormones.
There are some problems with this study, however.
It was not double-blind, the treatments were not
randomized, it used a small sample size of eight,
and while the subjects were instructed to fast, no
data was offered to confirm this, like blood sugar
levels. The study also did not look at the
possible mechanisms by which the HF diet lowered T
and fT levels.
It has been proposed in the literature that fatty
acids may bind SHBG. If this is true, then after
the fat is broken down from a high fat meal, a
corresponding increase in blood fatty acid levels
would occur, and less SHBG is available to bind
with T. This would then increase the percentage of
fT in the blood. However, since the percentage of
fT in this study did not change (the total amount
decreased, not the percentage of total T), this
could not have occurred. The researchers do offer
that the only way that the HF meal could have
affected T/fT levels was either by increasing the
clearance rate or decreasing the production rate.
The clearance rate would be determined by the rate
of uptake by tissues, the rate of T and fT
metabolized by the liver, and the rate of
excretion by the kidneys. While fatty acids do
attach to T and fT inside the body, there is no
data to say that this increases uptake into
tissues like skeletal muscle or that the event
could occur within four hours post-meal ingestion.
It would be unlikely that the fatty acids from the
meal could affect the liver enzymes involved in T
or its fractions so soon. It is possible that
ketones produced from the breakdown of the fatty
acids could cause the renal tubules to excrete
more T and fT. But this is unlikely due to the
fact that the subjects were not in a
glycogen-depleted state and there were PROs and
CHOs in the meal. This leaves decreased production
of T and fT as the most likely reason for the drop
in these hormones. Again, this is only speculation
at this point since the study did not examine the
possible causes for the decrease in the hormones.
Chronic Effects of Dietary Fat on Testosterone
The chronic studies presented in Table 3 report
the effects of 2 or more weeks of dietary
manipulations on testosterone levels. A decrease
in dietary fat has been shown to decrease total T
(8, 11, 15) and fT levels (8, 16) or not affect T
levels (17). Approaching this from the other
direction, an increase in dietary fat has been
shown to decrease total T (11), and increase (16)
or decrease fT levels (6). It’s not necessary to
review all the studies to try to explain the
differences in results. However, notice that from
the Table 3, most studies compared vegetarian-type
diets to western-type diets. This presents several
problems when trying to explain the hormonal
responses from the dietary manipulations. The
first is that other dietary factors were altered
in addition to fat intake. These included fiber
content and the presence of various phytonutrients
like flavonoids, isothiocyanates, etc. The main
point is that there are many factors that can
determine the effects of dietary fat on T levels.
Most studies did not even report the amounts of
fatty acids in the subjects’ diets, let alone the
content of phytonutrients, so these factors were
most likely not controlled for. Furthermore,
differences in the length of the treatments (2
weeks vs. 10 weeks), lifestyles of the subjects
(active vs. sedentary), and calorie loads (2800
vs. 4374) are additional examples of factors that
can impact the results.
All the Evidence Not In Yet
It has been speculated that the ratio of fatty
acids may have some role on whether or not dietary
fat increases or decreases T levels. A positive
relationship between saturated fatty acids and
monounsaturated fatty acids with T levels has been
reported previously (19). The same data also
describes a negative (or inverse) relationship
between polyunsaturated fatty acids and T levels.
These relationships between dietary fat components
and T have also been supported by a study on eight
men randomly assigned and crossed over from a
vegetarian diet to a mixed-meat diet that was
isoenergetic (15). About 28% of the calories were
from fat. The vegetarian diet had a
polyunsaturated fatty acid to saturated fatty acid
ratio (P:S) > 1, while the mixed-meat diet had P:S
of about .5.
In a 1996 study, forty-three men were exposed to a
high-fat, low-fiber diet for 10 weeks and a
low-fat, high-fiber diet for 10 weeks in a cross
over design (6). Total T and fT did not change
significantly. SHBG-bound T was higher on the
high-fat diet, which does not agree with another
study (16). The researchers claimed this might
have been due to within-person variations of
plasma testosterone levels.
Another important finding was that urinary
excretion of T was much greater on the high-fat,
low-fiber diet (6). Other studies have shown that
on higher fat diets, urinary excretion of T is
increased (10, 11) while vegetarian type diets may
decrease the urinary excretion of T (9, 10, 11).
This is an important point to consider in
evaluating the level of T bioactivity in the body.
If blood levels of T elevate and the excretion
rate of T also elevates there may not be a net
bioactive effect of T. However, if blood levels of
T remain the same and T excretion decreases, that
may signal a net bioactive effect of T in the
body. While it is difficult to say if a higher fat
or lower fat diet would be better for increasing
the bioactivity of T, it does appear that higher
fat and lower fiber-type diets are associated with
greater excretion of T. An increase in the urinary
excretion of T combined with an elevation of T
levels in the blood may indicate that the net T
production is greater. The implication is that
cells may have an increased opportunity to be
exposed to T. Alternatively, perhaps it is the
result of some type of self-regulating mechanism
that the body maintains to keep endogenous levels
in check.
There are many more studies in the literature. The
intent was to expose the reader to all the
different possible interactions and the complexity
in trying to control for all areas just to
determine the role of fat on androgen production.
Other studies have examined the effects of
different fatty acids on testicular cell membranes
and T levels after supplementation fatty acid
supplementation. The results do not support one
another and only point to the fact that dietary
fat plays a role in modifying T production, but
that role is still unclear.
Designing A Diet to Maximize Testosterone Levels
Remember, it is the bioactive fraction of total T
that is important. This fraction consists of fT
and albumin-bound T. Fasting suppresses T
production and small amounts of either PRO or CHO
do not reverse the suppression. Diets with a PRO
intake greater than the CHO intake lower total T
levels, and may actually decrease the bioactivity
of T in the body. Higher CHO diets (70% or more
from CHOs) may increase T levels, but they also
affect the metabolism of T as well. While the role
of fat is not entirely clear, saturated fat and
cholesterol are closely linked to higher levels of
T and PUFAs have some modifying role.
So, what is the best type of diet to follow if
your only concern is to increase T levels and make
more of it available to the body for the purpose
of improving lean body mass and/or performance? It
would seem that CHO intake must exceed PRO intake
by at least 40% to keep the bioactive fraction of
T high. Fat intake should be at least 30%,
saturated fat needs to be higher than PUFA, and
fiber intake needs to be low. A sample diet would
have roughly the following calorie breakdown: 55%
CHO, 15% PRO and 30% fat. On the other hand, what
if you wanted to lower your T levels in order to
minimize cardiovascular disease risk factors
and/or hormone-dependent cancer risks? Then a diet
with more protein, more fiber, a fat intake below
25%, and a P:S ratio of 1 or higher would be a
more prudent choice. The breakdown of this sample
diet would be about 50% CHO, 30% PRO and 20% fat.
The problem with using percentages, however, is
that people with high calorie needs will most
likely take in far more protein then they need.
Calories and Protein
by Thomas Incledon and Lori Gross
Introduction
This article will be divided into two parts. Part
1 presents an overview of how testosterone is
stimulated in the body, shows how calorie balance
affects T production, and discusses how dietary
protein intake affects circulating T levels. Part
2 explains how carbohydrates and fats impact
testosterone synthesis and circulation, and then
puts it all together for you to make informed
decisions. Keep in mind that this is a very
complicated and dynamic process. References will
be limited primarily to studies on men. However,
animal research will be cited when it becomes
necessary to discuss proposed mechanisms, or how
the actual changes in the body take place. While
the information may get technical at times, read
on because you will learn a great deal that you
may wish to apply to your own diet.
The HPT Axis
An article on the effects of diet on hormones
would be incomplete without a basic overview of
the relationships between the organs and hormones
of the axis. The term axis simply refers to the
pathway in question. The glands of this pathway
include the hypothalamus, pituitary, and testes.
The sequence of events culminating with the
production and/or release of T begins at the
hypothalamus. Here specialized nerve cells release
a hormone called gonadotropin-releasing hormone
(GnRH). GnRH is a decapeptide (chain of ten amino
acids) that travels by direct blood vessel
connections to the anterior pituitary where it
stimulates the release of luteinizing hormone (LH)
(1). LH is then secreted into the blood where it
attaches to receptors on the Leydig cells of the
testes. This induces activity of an enzyme,
P-450scc, referred to as the
cholesterol-side-chain-cleavage enzyme (1).
Through a series of five enzymatic steps,
cholesterol is converted into T.
The body regulates the circulating blood levels of
T via several mechanisms. Once in the blood, about
44% of T is bound to a protein called either
sex-hormone-binding-globulin (SHBG) or
testosterone-binding globulin (TeBG), to indicate
the greater affinity for T over estradiol (E2, an
estrogen). About 54% of T is bound by albumin and
other proteins, leaving 2% to circulate unbound to
any protein. This unbound T is termed free
testosterone (fT) (1). It is currently believed
that only the fT or albumin bound T are truly
available to interact with the tissues of the
body. The significance of this point will be
elaborated upon later in reviews of the data from
different studies. Of the T that is available to
interact with tissues, some of it binds to steroid
receptors. In most tissues, like skeletal muscle,
it will directly stimulate protein synthesis. In
some tissues, like the brain and fat cells, it can
be converted into E2 via the aromatase enzyme. In
other tissues, like the prostate gland, it can be
converted into dihydrotestosterone (DHT) via the
5-alpha-reductase enzyme. T either directly or
through conversion to E2 or DHT can inhibit its
own future production. The conversion to E2 or DHT
can take place both in the brain and various other
tissues. E2 and T exert stronger inhibitory
effects than DHT on T production. This process is
called negative-feedback inhibition. This is the
reason why the use of steroids, enzyme inhibitors,
and prohormones are far from perfect in their
effects on increasing T levels. Because it is a
dynamic process, as T levels elevate in the blood,
a corresponding increase in inhibitory signals
occurs. This results in the body making less T.
The opposite occurs when T levels decrease. This
is a basic overview and presented in a simplistic
static fashion. The body is a highly dynamic
organism and many factors come into play to help
regulate this process. This point is made to
illustrate the confounding problem that occurs
when trying to increase circulating levels of
androgens.
Effects of Calorie Intake on Testosterone
Every minute of the day, someone makes a decision
to lose weight. Dieting by means of restricting
calories, while not always successful, is
practiced frequently. There are some people who
believe that fasting (or what we call planned
starvation) is a necessary method for cleaning the
body of wastes. What effects does depriving the
body of calories have on endocrine responses
within the HPT axis? As you may have already
guessed, it screws things up. Fasting for 5 days
can lower LH, T, and fT by 30-50% (2). What
appears to happen is that as the body becomes
deprived of energy, less GnRH is released from the
hypothalamus. This, in turn, leads to a weaker
signal to release LH. While the pattern of LH
release remains the same, the amount of LH
released at each interval decreases, meaning your
body is giving weaker signals to stimulate T. In
addition, research on fasting in rats indicates
that testicular enzymes involved in synthesizing T
decrease in function (3). This means that even if
enough LH reaches the testes, they still cannot
produce normal amounts of T. The decrease in T can
be a contributing factor to the loss in lean body
mass that occurs with fasting. Of course, this is
contrary to what most of us want to do in the
quest to get bigger and stronger. However, many
elite athletes have learned how to apply fasting
to their contest preparation. Fasting before a
drug test is a common practice when on
anabolic-androgenic steroids because it helps
prevent testing positive. But before you run out
and load up on some "juice" and think you’ll beat
a drug test just by fasting, keep in mind that
this method is not always reliable, nor does it
work when you have foreign metabolites in the
body.
One of the common problems when dieting is holding
onto all that hard earned muscle. Severe calorie
restriction, whether from reduced food intake or
imposed by excessive exercise, lowers testosterone
(4). While there are no numbers written in stone,
a decrease in calories by 15% does not lower T
levels (5). This may serve as one factor to
consider when planning out a diet strategy. If you
cut back too much on your calories, then you risk
lowering your T, which can cause you to say
goodbye to some of your muscle. The good news is
that when refeeding resumes and calorie intake
equals calorie expenditure, in most cases, T
levels will rise back to normal. The bad news is
that if you are engaging in chronic high volume
endurance exercise, even extra calories won’t help
raise your T levels back to normal.
When male subjects are overfed in an attempt to
induce weight gain, there tends to be a decrease
in T levels as upper body fat increases (6). It
may be wise, therefore, to limit calorie intakes
to less than 1000 Calories (kilocalories) above
energy requirements. From reviewing the
literature, it seems that with large short-term
increases in body fat and small chronic increases,
T levels go down. Perhaps this is due to an
inverse relationship between T and insulin and/or
the aromatase enzyme. It is clear that with
excessive body fat, aromatase activity in fat
cells increases, thus more of T is converted into
an estrogen called estradiol (E2). The issue with
insulin is far more complicated and not really
clear. Some research has shown insulin to regulate
T in a positive fashion (7), while carbohydrate
and protein liquid meals, which elevate insulin,
have been shown to decrease T in resistance-
trained males (8,9). This may be due to an
increased uptake by tissues, like skeletal muscle,
increased excretion of T in the urine, or
decreased responsiveness of the testes to produce
T.
While not related to caloric intake, hydration and
sleep status are also important. A reduction of
3.8% in body weight due to dehydration did not
affect T levels during mild exercise (10). But,
don’t take any chances with hydration. Drink
plenty of water every day at the rate of 30 cc per
kilogram of body weight (or roughly one ounce for
every two pounds). Get plenty of sleep, as
disturbances in sleep and light/dark cycles can
decrease T by almost 50% (11). Of course, no one
ever gets enough sleep!
Dietary Protein Intake & Testosterone
The direct impact of protein by itself on T levels
has not been well studied in humans. Some research
on high protein diets deals with the effects on
very obese people and weight loss. While this may
not seem applicable to you, read on and we will
put it together for you. In obese men, feeding 600
calories a day with 400 calories from protein (50
grams of beef protein and 50 grams of casein)
induces lower levels of T than fasting does (12).
Normally, when the kidneys filter T out of the
blood, some T gets reabsorbed back out of the
kidneys into the blood. The researchers stated
that the additional protein in the diet generated
more ketones. They concluded that the ketones were
filtered out of the blood by the kidneys and were
reabsorbed back into circulation preferentially
over T. While most people reading this may not be
obese, higher protein diets are definitely in
vogue, more so for bodybuilders and powerlifters
than other groups of athletes. The potential
exists that if a ketogenic diet like the Atkins
Diet or a cyclical ketogenic diet like the
Anabolic Diet or Bodyopus is followed, than
urinary excretion of T will be greater during the
ketogenic phase of the diet.
It is known that protein in the diet can influence
the metabolism of a variety of chemicals. Through
a series of experiments, it was demonstrated that
various foods could influence the metabolism of
drugs in the body (13). Vegetables like cabbage
and brussel sprouts were found to alter the
function of specific liver enzymes. This, in turn,
could change the half-life of a drug in the blood.
Given the variety of diets that people follow and
the variety of prescription medications and
over-the-counter drugs people take, the logical
progression was to look at how altering the
macronutrient composition of the diet affected
drug metabolism. It turns out that a higher ratio
protein diet, a diet with more calories from
protein than carbohydrates or fat, metabolizes
some drugs faster, thus decreasing the clearance
time of the drug. Since diet can affect drug
metabolism, perhaps it could affect liver enzymes
involved in the metabolism of endogenous steroids.
Sure enough, it was found that a high ratio
protein diet decreased the reduction of T (14).
Reducing the reduction of T could mean a potential
decrease in DHT and/or androsterone in the blood,
which is good by most accounts. However, DHT
levels were not measured and, more importantly,
urinary T excretion increased, although it was not
statistically significant. These subjects were not
in ketosis, so perhaps ketones do not increase T
excretion rates. Regardless of the exact
mechanism, there is sufficient evidence in the
literature that when protein intake exceeds
carbohydrate intake, T clearance increases by
excretion in the urine.
A cross over design study used seven normal men
from 23-43 years of age and compared a high
protein diet to a high carbohydrate diet (15).
This study has been referenced many times and
cited as proof that high protein diets lower total
T levels in the blood. The high carbohydrate diet
from this study will be covered in Part II. The
high protein diet consisted of 44% protein, 35%
carbohydrate, and 21% fat and supplied between
2400 and 2500 kilocalories per day (kcals/d).
Let’s assume it was an even 2450 kcals/d. The men
also had bodyweights that ranged from 64-72 kg. If
we assume the mean was 68 kg, then this would give
us an average body weight of about 150 pounds.
This means these guys were eating [(2450 kcals/d
times .44) (divide by 4)] 270 grams (g) of
protein, [(2450 x.350 /4] 215 g of carbohydrates
(CHO) and [(2450 x .21) /9] 58 g of fat per day.
However, total T is not that big of a deal. The
more important measure is the bioactive fraction
of T. (Earlier in the overview of the HPT Axis, it
was mentioned that SHBG-bound T is not considered
bioactive, while the other fractions of T are).
While subjects followed the high protein diet,
their total T levels were 28% lower than on the
higher CHO diet (15). This is important because T
decreased in all seven subjects, although the
magnitudes of the decrease ranged from 10 to 93%.
For the same seven subjects, their SHBG levels
decreased about 39% with a range from 19 to 64%.
Looking at this data gives the impression that the
actual bioactivity of T was higher while the
subjects were on a high protein diet. SHBG-bound T
and fT were not measured, so it is not known for
sure. On the surface it appears that a mean
decrease of 39% in the SHBG values and only a 28%
in the T would leave more T available for binding
to tissues. However, if we calculate out the
actual changes in the hormones using the data from
the study, we see something different. The mean
and standard error (M±SE) for T was 371 ± 23
ng/dL. The currently used units in clinical
chemistry are nmol/L. Multiplying the mean T by
the conversion factor of 0.0347 gives us about
12.9 ± .8 nmol/L. The M±SE SHBG was 23.4 ± 1.6
nmol/L. If we assume that the amount of T bound to
SHBG averages 44%, then .44 x 12.9 ± .8 nmol/L
gives us 5.7 ± .4 nmol/L of T bound to SHBG. That
leaves 7.2 ± .4 nmol/L of T to interact with
tissues in the body. However, we don’t know from
the data if the amount of SHBG bound T decreased
below or increased above the normal 44%, in which
case there would be more or less T available to
interact with tissues.
From work by the same group of researchers using
the exact same diet (but different subjects) we
see that the ratio of 5a - reduction to 5b -
reduction (5a /5b ) of T is reduced by about 50%,
with the decrease being attributed to lower rates
of 5a - reduction (14). The T values that have
been used thus far (15) already reflect any
changes in altered T metabolism, so the conversion
to a 5a - reduced hormone (ie androsterone) is
accounted for at this point. Note that even though
there is a decrease in 5a - reduced hormone
production, it does not show up as increased T
levels. The decrease in androsterone probably
shows up in small, but statistically insignificant
increases in other metabolites of T (they were
statistically insignificant perhaps due to the
small sample size). Another interesting aspect is
that there is an increase in the oxidation of
estradiol on the higher protein diet by about
14-15% (14). Unfortunately estradiol levels were
not measured in this paper. This could have given
us clues as to the mechanism by which higher
protein diets lower T (ie increased negative
feedback on T levels via estradiol). At this
point, this is only one study and it is still
difficult to come to any final conclusions.
However, if this is what really happens, then a
high-protein diet may actually lower the anabolic
actions of T in the body. Unfortunately, this has
not been verified through laboratory research and
is just a theory at this point. Perhaps the
decrease in T is a result of increased excretion
in the urine either as T or a sulfated metabolite,
or increased conversion to estradiol and oxidation
by the liver.
Prelude to the Effects of Diet on Testosterone
Part II: Carbohydrates and Fat
We hope so far that you have learned something
about testosterone production and the effects of
calorie intake and protein intake on testosterone
levels in the blood. Please feel free to contact
us if you have any questions or comments at
lorig8r@sprynet.com . In the next article, the
effects of carbohydrates and fat and total T
levels and its components are explained. We will
then review the key points and see how the
information can be integrated into a diet
strategy. At this point we would like to thank
Albert Jenab for his technical assistance and
insight.
References
1) Griffin JE. & Ojeda SR, editors of: Textbook of
Endocrine Physiology, 3rd edition. New York,
Oxford University Press, 1996.
2) Aloi JA. Bergendahl M. Iranmanesh A. Veldhuis
JD. Pulsatile intravenous gonadotropin-releasing
hormone administration averts fasting-induced
hypogonadotropism and hypoandrogenemia in healthy,
normal weight men. Journal of Clinical
Endocrinology & Metabolism. 82(5):1543-8, 1997
May.
3) Fanjul LF. Ruiz de Galarreta CM. Effects of
starvation in rats on serum levels of
testosterone, dihydrotestosterone and testicular 3
beta-hydroxysteroid dehydrogenase activity.
Hormone & Metabolic Research. 13(6):356-8, 1981
Jun.
4) Marniemi J. Vuori I. Kinnunen V. Rahkila P.
Vainikka M. Peltonen P. Metabolic changes induced
by combined prolonged exercise and low-calorie
intake in man. European Journal of Applied
Physiology & Occupational Physiology. 53(2):121-7,
1984.
5) Garrel DR. Todd KS. Pugeat MM. Calloway DH.
Hormonal changes in normal men under marginally
negative energy balance. American Journal of
Clinical Nutrition. 39(6):930-6, 1984 Jun.
6) Pritchard J. Despres JP. Gagnon J. Tchernof A.
Nadeau A. Tremblay A. Bouchard C. Plasma adrenal,
gonadal, and conjugated steroids before and after
long-term overfeeding in identical twins. Journal
of Clinical Endocrinology & Metabolism.
83(9):3277-84, 1998 Sep.
7) Pasquali R. Macor C. Vicennati V. Novo F. De
lasio R. Mesini P. Boschi S. Casimirri F. Vettor
R. Effects of acute hyperinsulinemia on
testosterone serum concentrations in adult obese
and normal-weight men. Metabolism: Clinical &
Experimental. 46(5):526-9, 1997 May.
8) Kraemer WJ. Volek JS. Bush JA. Putukian M.
Sebastianelli WJ. Hormonal responses to
consecutive days of heavy-resistance exercise with
or without nutritional supplementation. Journal of
Applied Physiology. 85(4):1544-55, 1998 Oct.
9) Chandler RM. Byrne HK. Patterson JG. and Ivy
JL. Dietary supplements affect the anabolic
hormones after weight-training exercise. Journal
of Applied Physiology. 76(2): 839-845, 1994 Feb.
10) Hoffman JR. Maresh CM. Armstrong LE. Gabaree
CL. Bergeron MF. Kenefick RW. Castellani JW.
Ahlquist LE. Ward A. Effects of hydration state on
plasma testosterone, cortisol and catecholamine
concentrations before and during mild exercise at
elevated temperature. European Journal of Applied
Physiology & Occupational Physiology.
69(4):294-300, 1994.
11) Cortes-Gallegos V. Sojo Aranda I. Gio Pelaez
RM. Disturbing the light-darkness pattern reduces
circulating testosterone in healthy men. Archives
of Andrology. 40(2):129-32, 1998 Mar-Apr.
12) Hoffer LJ. Beitins IZ. Kyung NH. Bistrian BR.
Effects of severe dietary restriction on male
reproductive hormones. Journal of Clinical
Endocrinology & Metabolism. 62(2):288-92, 1986
Feb.
13) Anderson KE. Conney AH. Kappas A. Nutrition as
an environmental influence on chemical metabolism
in man. Progress in Clinical & Biological
Research. 214:39-54, 1986.
14) Kappas A. Anderson KE. Conney AH. Pantuck EJ.
Fishman J. Bradlow HL. Nutrition-endocrine
interactions: induction of reciprocal changes in
the delta 4-5 alpha-reduction of testosterone and
the cytochrome P-450-dependent oxidation of
estradiol by dietary macronutrients in man.
Proceedings of the National Academy of Sciences of
the United States of America. 80(24):7646-9, 1983
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15) Anderson KE. Rosner W. Khan MS. New MI. Pang
SY. Wissel PS. Kappas A. Diet-hormone
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__________________
The Effects of Diet on Testosterone (Part 2):
Carbohydrates and Fats
by Thomas Incledon and Lori Gross
Introduction
Part One of this article explained the impact of
calories and dietary protein (PRO) on endogenous
testosterone (T) levels. As promised, this
continuation will focus on the role of dietary
carbohydrates (CHO) and dietary fat on modulating
T production. The role of CHO on T production is
indirectly addressed when discussing the role of
PRO or fat, so this will be reviewed briefly. The
effects of fat on T are far more complicated and
often time more confusing than the previously
discussed macronutrients. To facilitate an
understanding of the links between dietary fats or
lipids and T, several tables will be presented. An
explanation will accompany each table and key
references will be reviewed. The article ends with
an application of the information to the design of
a dietary strategy to either maximize or minimize
T levels.
Dietary Carbohydrate Intake & Testosterone
Dietary carbohydrates can influence the metabolism
of a variety of chemicals. When fat is held at
approximately 20% of caloric intake, CHO may
elevate T levels (1). Part One of this article
discussed that while this may be true, there is
also a corresponding increase in sex hormone
binding-globulin (SHBG). Anderson et al (1)
compared the effects of a higher PRO diet versus a
higher CHO diet on T levels. Part one discussed
the data on the high protein diet. The higher CHO
diet contained approximately 2450 kcals/d, 70%
CHO, 10% PRO, 20% fat. This provides 429 g/d CHO,
62 g/d PRO, and 55 g/d fat. The seven men in this
study had a range of body weights from 64-72 kg.
If a mean of 68 kg is assumed, then these subjects
were taking in .91g PRO/kg BW or slightly higher
than the RDA of .8g/kg BW. This point is made
because most people take in more protein than this
on a daily basis.
Now let’s get back to the T and SHBG issue. The
interaction between T and SHBG is important to
consider. About 44% of total T is bound to SHBG
and is called SHBG-T. If T increases more than the
SHBG-T fraction does, then the biological actions
of T will be greater because more of it will be
available to bind to muscle and other tissues’
receptors. If T increases less than SHBG-T
fraction, then the biological actions of T will
decrease because less of it will be available to
bind to muscle and other tissues’ receptors.
Anderson et al did not measure SHBG-T. The study
did measure total T and SHBG. It can be seen from
their data, that T increases less than SHBG did on
the higher CHO diet with a ratio of 7:1 (CHO:PRO).
The T values were 16.2 ± 1.2 nmol/L. This was a
28% increase over the high PRO diet and the range
of increases in the subjects was from 10-93%.
Assuming that the SHBG-T fraction remained at 44%
of T, then the amount of T that was bioavailable
would be about 9.1 ± .66 nmol/L. Compared to the
amount of bioavailable T on the high PRO diet,
there is an additional 1.9 ± .21 nmol/L of
bioavailable T.
Also keep in mind that this same type of diet
increases the ability of the liver to reduce T to
5a - reduced hormones (ie androsterone) (2), which
may or may not be something you want (depending on
the study you read). However, this is especially
important for steroid and prohormone users because
a higher CHO diet may increase the conversion of
the exogenous T to androsterone. This is not to
say that diets with higher CHO than PRO will cause
this to occur. What this means is that very high
CHO:PRO ratios like 7:1 or greater may not be the
healthiest way to go, based upon direct and
indirect evidence that androsterone is linked to
acne and prostate disorders.
The effects of CHO on T were just discussed while
fat was kept constant in the diet at about 20% of
calories. When PRO is kept constant in the diet,
higher CHO may actually lower T (8). Hamalainen et
al (8) compared the effects of a dietary
intervention on the hormone levels of 30 men. PRO
intake was fairly consistent while the CHO was
increased from 45% to 56% of calories for six
weeks, and then decreased to 47% for six weeks.
Fat intake was correspondingly decreased from 40%
to 25%, and then increased to 37%. During the
higher CHO period, T and fT decreased
significantly. However, this study was difficult
to interpret because dietary fibers, like pectin
from fruit or bran from wheat, and fatty acids,
like saturated fatty acids or polyunsaturated
fatty acids, can also have an impact on T
production. In the Hamalainen et al study, they
also changed the fatty acid ratios of the diets.
Perhaps the ratio of fatty acids, as opposed to
the amount of CHO or fat, had a larger impact on T
production. Extrapolating this further, maybe it
is not the amount of CHO or the CHO:PRO that
influences T production, but the ratio of CHO to a
particular fatty acid, or some other nutrient
interaction (ie PRO to fatty acid or ratio of
fatty acids).
Correlation Studies Between Dietary Fat Intake and
Testosterone Levels in Men
Fat has received tremendous attention over the
last few years and has been linked to improved
performance and favorable body composition
alterations in the lay journals, despite a lack of
convincing scientific data. The relationship
between dietary lipids and T is important in order
to understand the role that fat may have in
improving performance, altering body fat, or
preventing/initiating disease.
One of the reasons why the scientific data has not
been clear in explaining the role of dietary fat
on T levels is a difference in study designs.
Table 1 displays the data and results from several
studies that compared T, free testosterone (fT),
and/or SHBG levels with total fat or types of
fatty acids in the diet. Data is listed as the
mean values (when available). Correlation studies,
while very common, are far from complete. They
don’t explain if dietary fat or some fraction,
like polyunsaturated fatty acids (PUFA), affects
T, rather they only state if there is a
relationship between one event and another. The
relationship can be positive and an example of
this is reference 19 from Table 1. From the
results column the code FCT is listed in the
results column. FCT means that as the percentage
of calories from fat, grams of saturated fat, and
grams of monounsaturated fat (MUFA) increased in
the diet, there was also a corresponding
association with higher T levels. This study was
done with resistance trained males and is the most
applicable from all of the above studies. The
scope of this article precludes an in-depth
analysis of each study and the associated design
flaws. Most important is to cite the common
findings. From Table 1, several relationships can
be seen. Subjects consuming vegetarian diets have
demonstrated higher SHBG levels (3, 13), lower T
levels (12), and lower levels of available T (3).
One flaw with many of these studies is isolating
the impact of fat on the diet as opposed to fiber,
which is also much higher in vegetarian-type
diets. Another problem with correlational studies
is that they don’t tell you what happens when
subjects are switched from one type of diet to
another. Unfortunately studies sometimes
contradict each other. For example, Bishop et al
(4) examined the role of dietary nutrients on sex
hormone differences between monozygotic twins
(identical twins). The investigators found an
inverse (or negative) relationship between dietary
fats and T. Volek et al (17) however, found a
positive relationship between dietary fat and T.
This further demonstrates the problem of reading
the scientific literature and making sense of all
the information.
Acute Effects of Dietary Fat on Testosterone
A better study design than a correlational study
to determine the effects of manipulating dietary
macronutrients is a randomized cross over,
double-blind study. Cross over means that every
subject experiences all of the different dietary
treatments. By randomizing the order, the effect
of one diet on another is avoided (this is called
order effect). Double-blind means that the
subjects, the people working with the subjects,
and the people tracking the data are all unaware
of the treatment conditions. This is very
difficult to do with feeding studies, so in most
cases a double-blind approach is not used.
Therefore, in most studies, the subjects and/or
the researchers know what the treatment conditions
are. One way the researchers avoid this problem is
to offer milk shakes that taste the same, but, in
fact, have different macronutrient compositions.
While this may be acceptable to study the acute
effects of more or less fat in a meal, this would
not work for chronic studies. After all, could you
drink the same milkshake all day long for weeks
and weeks, or worse yet eat some type of
engineered food product not knowing what was
inside?
Acute studies examine the effects of different
treatments within the hours or days after the
dietary manipulation. In general, the subjects are
given different types of diets and the results of
each diet are compared. This is one way to look at
the effects of a particular nutrient on hormone
levels or blood glucose levels, for example. Table
2 presents the tabulated data from two short term
or acute studies.
In one study (14), the effects of high fat (HF)
and low fat (LF) meals on T levels were compared.
The subjects were given a lemon-lime artificially
sweetened beverage and the hormonal responses
served as a control © for the other meals. A HF
liquid meal containing about 795 calories and made
up of 57% fat (50.4 g fat), 9% protein (17.9 g
PRO), and 34% carbohydrate (67.5 g CHO) was given
on another occasion. The third or final liquid
meal (LF) consisted of 797 calories made up of
1.2% fat (1 g fat), 25.5 % PRO (51 g PRO), and
73.3% CHO (146 g of CHO). The C and LF meals did
not effect luteinizing hormone (LH), T, fT or
dihydrotestosterone (DHT) levels. The HF meal
decreased T and fT up to 4 hours post ingestion
compared to the other liquid meals without
affecting any of the other hormones.
There are some problems with this study, however.
It was not double-blind, the treatments were not
randomized, it used a small sample size of eight,
and while the subjects were instructed to fast, no
data was offered to confirm this, like blood sugar
levels. The study also did not look at the
possible mechanisms by which the HF diet lowered T
and fT levels.
It has been proposed in the literature that fatty
acids may bind SHBG. If this is true, then after
the fat is broken down from a high fat meal, a
corresponding increase in blood fatty acid levels
would occur, and less SHBG is available to bind
with T. This would then increase the percentage of
fT in the blood. However, since the percentage of
fT in this study did not change (the total amount
decreased, not the percentage of total T), this
could not have occurred. The researchers do offer
that the only way that the HF meal could have
affected T/fT levels was either by increasing the
clearance rate or decreasing the production rate.
The clearance rate would be determined by the rate
of uptake by tissues, the rate of T and fT
metabolized by the liver, and the rate of
excretion by the kidneys. While fatty acids do
attach to T and fT inside the body, there is no
data to say that this increases uptake into
tissues like skeletal muscle or that the event
could occur within four hours post-meal ingestion.
It would be unlikely that the fatty acids from the
meal could affect the liver enzymes involved in T
or its fractions so soon. It is possible that
ketones produced from the breakdown of the fatty
acids could cause the renal tubules to excrete
more T and fT. But this is unlikely due to the
fact that the subjects were not in a
glycogen-depleted state and there were PROs and
CHOs in the meal. This leaves decreased production
of T and fT as the most likely reason for the drop
in these hormones. Again, this is only speculation
at this point since the study did not examine the
possible causes for the decrease in the hormones.
Chronic Effects of Dietary Fat on Testosterone
The chronic studies presented in Table 3 report
the effects of 2 or more weeks of dietary
manipulations on testosterone levels. A decrease
in dietary fat has been shown to decrease total T
(8, 11, 15) and fT levels (8, 16) or not affect T
levels (17). Approaching this from the other
direction, an increase in dietary fat has been
shown to decrease total T (11), and increase (16)
or decrease fT levels (6). It’s not necessary to
review all the studies to try to explain the
differences in results. However, notice that from
the Table 3, most studies compared vegetarian-type
diets to western-type diets. This presents several
problems when trying to explain the hormonal
responses from the dietary manipulations. The
first is that other dietary factors were altered
in addition to fat intake. These included fiber
content and the presence of various phytonutrients
like flavonoids, isothiocyanates, etc. The main
point is that there are many factors that can
determine the effects of dietary fat on T levels.
Most studies did not even report the amounts of
fatty acids in the subjects’ diets, let alone the
content of phytonutrients, so these factors were
most likely not controlled for. Furthermore,
differences in the length of the treatments (2
weeks vs. 10 weeks), lifestyles of the subjects
(active vs. sedentary), and calorie loads (2800
vs. 4374) are additional examples of factors that
can impact the results.
All the Evidence Not In Yet
It has been speculated that the ratio of fatty
acids may have some role on whether or not dietary
fat increases or decreases T levels. A positive
relationship between saturated fatty acids and
monounsaturated fatty acids with T levels has been
reported previously (19). The same data also
describes a negative (or inverse) relationship
between polyunsaturated fatty acids and T levels.
These relationships between dietary fat components
and T have also been supported by a study on eight
men randomly assigned and crossed over from a
vegetarian diet to a mixed-meat diet that was
isoenergetic (15). About 28% of the calories were
from fat. The vegetarian diet had a
polyunsaturated fatty acid to saturated fatty acid
ratio (P:S) > 1, while the mixed-meat diet had P:S
of about .5.
In a 1996 study, forty-three men were exposed to a
high-fat, low-fiber diet for 10 weeks and a
low-fat, high-fiber diet for 10 weeks in a cross
over design (6). Total T and fT did not change
significantly. SHBG-bound T was higher on the
high-fat diet, which does not agree with another
study (16). The researchers claimed this might
have been due to within-person variations of
plasma testosterone levels.
Another important finding was that urinary
excretion of T was much greater on the high-fat,
low-fiber diet (6). Other studies have shown that
on higher fat diets, urinary excretion of T is
increased (10, 11) while vegetarian type diets may
decrease the urinary excretion of T (9, 10, 11).
This is an important point to consider in
evaluating the level of T bioactivity in the body.
If blood levels of T elevate and the excretion
rate of T also elevates there may not be a net
bioactive effect of T. However, if blood levels of
T remain the same and T excretion decreases, that
may signal a net bioactive effect of T in the
body. While it is difficult to say if a higher fat
or lower fat diet would be better for increasing
the bioactivity of T, it does appear that higher
fat and lower fiber-type diets are associated with
greater excretion of T. An increase in the urinary
excretion of T combined with an elevation of T
levels in the blood may indicate that the net T
production is greater. The implication is that
cells may have an increased opportunity to be
exposed to T. Alternatively, perhaps it is the
result of some type of self-regulating mechanism
that the body maintains to keep endogenous levels
in check.
There are many more studies in the literature. The
intent was to expose the reader to all the
different possible interactions and the complexity
in trying to control for all areas just to
determine the role of fat on androgen production.
Other studies have examined the effects of
different fatty acids on testicular cell membranes
and T levels after supplementation fatty acid
supplementation. The results do not support one
another and only point to the fact that dietary
fat plays a role in modifying T production, but
that role is still unclear.
Designing A Diet to Maximize Testosterone Levels
Remember, it is the bioactive fraction of total T
that is important. This fraction consists of fT
and albumin-bound T. Fasting suppresses T
production and small amounts of either PRO or CHO
do not reverse the suppression. Diets with a PRO
intake greater than the CHO intake lower total T
levels, and may actually decrease the bioactivity
of T in the body. Higher CHO diets (70% or more
from CHOs) may increase T levels, but they also
affect the metabolism of T as well. While the role
of fat is not entirely clear, saturated fat and
cholesterol are closely linked to higher levels of
T and PUFAs have some modifying role.
So, what is the best type of diet to follow if
your only concern is to increase T levels and make
more of it available to the body for the purpose
of improving lean body mass and/or performance? It
would seem that CHO intake must exceed PRO intake
by at least 40% to keep the bioactive fraction of
T high. Fat intake should be at least 30%,
saturated fat needs to be higher than PUFA, and
fiber intake needs to be low. A sample diet would
have roughly the following calorie breakdown: 55%
CHO, 15% PRO and 30% fat. On the other hand, what
if you wanted to lower your T levels in order to
minimize cardiovascular disease risk factors
and/or hormone-dependent cancer risks? Then a diet
with more protein, more fiber, a fat intake below
25%, and a P:S ratio of 1 or higher would be a
more prudent choice. The breakdown of this sample
diet would be about 50% CHO, 30% PRO and 20% fat.
The problem with using percentages, however, is
that people with high calorie needs will most
likely take in far more protein then they need.