The Effects of Diet on Testosterone (Part 2): Carbohydrates and Fats
by Thomas Incledon and Lori Gross
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
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
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
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 (C) 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
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
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. Another strategy is to
keep protein intake the same (ie 1 gram per pound of BW) and then play
around with the fiber, SFA:PUFA ratio, CHO, and total fat contents of the
diet. Antioxidants are important additions when trying the higher fat diets.
Keep in mind there are many factors that affect T production and they
interact in a complex and seemingly unpredictable fashion. We invite
feedback and will respond to all questions, comments, etc. Several readers
have mentioned the idea of cycling a diet that maximizes T and then
switching back to a healthier type of diet. For those that do try this,
please let us know your results.
Anderson KE. Rosner W. Khan MS. New MI. Pang SY. Wissel
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