Minimum daily required fat intake

[Insight]

long post, cliffs at end.

There are lots of "minimum required" guidelines for daily fat intake that I see... 0.5 g/lb being the most common, sometimes going down to 0.35 g/lb LBM (Em's recommendation). Alan Aragon has similar guidelines laid out in his AARR "culking" series (I think Jan 09 was the issue).

The usual reasoning is that if you set fat much lower you start to lose your sh*t. If you set fat too low the diet becomes unreasonably unmanageable. As alan put it in girth control, "a small handful of nuts would zap your daily fat requirement and have you cursing the skies."

But there's supposedly other reasons as well - maintaining optimal levels of hormones and such. And my question is, how important or relevant is all of that?

For example, I'm down to 1600 cals/day now, and if I actually got 0.5g/lb of fat I'd basically end up at 50g carbs per day. 50g of carbs per day makes me feel like absolute sh*t - foggy, headaches, sluggishness, etc. I could probably push past it and get into ketosis but the question is - is it really necessary? Does a 1600 cal diet really have to be ketogenic to be "optimal?"

Because in this situation the increased fat intake is actually making things worse on general sanity. It forces carbs to be low, which is even more of a pain in the ass than forcing fat to be low (for me, anyway, being particularly "insulin sensitive"). It also has pretty sh*tty effects on gym performance, probably because of all of that damn glycogen stuff.

The main argument I could see for keeping fat high has to do with the GI. Less fat = quicker gastric emptying = sharper glycemic response. And we all know the long term effects on glucose metabolism of eating exceptionally high-GL diets. I think that for the average joe it's pretty good advice, but for us more educated people it's a bit simplistic. You can also slow digestion by eating more fiber, for example.

The other usual theory is that fat levels being high = increased test production. But my question is - how relevant is this, really? Do test levels really vary that much, and does it actually make a difference? Test boosters can raise your test levels a little bit too, but it usually isn't significant enough to have an effect. Does the same apply here?

Some more insight would be appreciated. It's very "trendy" these days to keep fat high and carbs low, but I'm curious if it's really necessary. Back in the days the idea of low-carbing it was seen as ridiculous, but now it's okay. But now low-fatting it is seen as ridiculous, and I wonder if it's also okay.

I need cliffs Mike please speed this up
- What is the actual "minimum required" daily fat intake level before stuff goes wrong?
- Is going as high as 0.35-0.5g/lb of fat per day really necessary, even if overall caloric intake is low enough that this leaves not much room for carbs (50g or so)?
- Re: more (unsaturated) fat being better for glucose metabolism - is this also relevant to folks like us who are aware of how glycemic levels change in response to a meal? We can also lower the glycemic response by eating more fiber or lower-GI carbs in general. This seems like a more useful guideline for the average guy eating too many refined carbs and who doesn't want to think about it.
- Re: more fat being better for test production - does this actually make a relevant difference on performance, body composition, etc? Jamie Hale has an article on how even among the drugged population, there's a "minimum threshold dose" of test you need to get to even see any difference. He uses this argument to assert that this is why test boosters are useless - even if they raise test levels it usually isn't enough for that to actually do anything. In light of this, is dietary fat's effect on test here really that extreme?

Any insight would be appreciated.

Sincerely,
#1 bro

[AbAbber2k]

The effects of dietary fats on test levels is likely similar to that of other test boosting supplements. A low fat diet may result in low test levels... increasing fat should normalize them... but it's unlikely that a high-fat diet would result in above normal test levels.

Your concerns regarding glycemic load are unfounded (unless you're diabetic or something), and there is no reason for you to have to consider keto (though I have no problems with keto diets). That said, your response to low-carbing is likely also partly the result of your unnecessarily low calorie intake. I'm going to assume for a moment that at 160, you're about 13% BF. That puts your BMR at around 1700... adjust for activity level and you're looking at a total need of 2400-2700 calories per day... on a 1600 calorie diet you are 700-1000 calories below maintenance. Based on your BF%, your maximum fat burn is going to be about 600cal/day (around a lb of fat loss per week)... which still leaves 100-400 calories unaccounted for... that's all going to come from blood/liver glycogen and probably muscle tissue... making you feel tired and lethargic most likely.

[Insight]

The effects of dietary fats on test levels is likely similar to that of other test boosting supplements. A low fat diet may result in low test levels... increasing fat should normalize them... but it's unlikely that a high-fat diet would result in above normal test levels.

Your concerns regarding glycemic load are unfounded (unless you're diabetic or something), and there is no reason for you to have to consider keto (though I have no problems with keto diets). That said, your response to low-carbing is likely also partly the result of your unnecessarily low calorie intake. I'm going to assume for a moment that at 160, you're about 13% BF. That puts your BMR at around 1700... adjust for activity level and you're looking at a total need of 2400-2700 calories per day... on a 1600 calorie diet you are 700-1000 calories below maintenance. Based on your BF%, your maximum fat burn is going to be about 600cal/day (around a lb of fat loss per week)... which still leaves 100-400 calories unaccounted for... that's all going to come from blood/liver glycogen and probably muscle tissue... making you feel tired and lethargic most likely.

I'm closer to 15% bf and 1600 is not "unnecessarily low" for me at all. It has me losing 1 lb/week. Having to drop own to 10 cals/lb to lose at 1 lb/week after long bouts of dieting is not unheard of.

[ErikTheElectric]

Great Read Insight!

Thanks for this

Repped. :)

[rgurleyjr]

I wish I could answer your questions, just wanted to say that my average fat intake is around 35-40 grams and I weigh 175. I'm curious if an intake that low is unhealthy? Personally, I'd rather have a lower fat intake and higher carb intake. I don't know understand why people are against carbs these days?

[rgurleyjr]

I just found out dietary cholesterol affects T production as well, I never knew that before. Anyways, I have to go to bed and haven't had time to completely read this but there are multiple references at the bottom. I'll check it out tomorrow.


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

rcise. Journal of Applied Physiology. 82(1): 49-54, 1997 Jan.

[rgurleyjr]

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 (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 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.

[rgurleyjr]

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. 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. lorig8r@sprynet.com.
References

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.

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.

Belanger A, A Locong, C Noel, et al. Influence of diet on plasma steroid and sex plasma binding globulin levels in adult men. Journal of Steroid Biochemistry. 32(6): 829-833, 1989.

Bishop DT, AW Meikle, ML Slattery, et al. The Effect of Nutritional Factors on Sex Hormone Levels in Male Twins. Genetic Epidemiology. 5:43-49, 1988.

Deslypere JP & A Vermeulen. Leydig cell function in normal men: effect of age, lifestyle, residence, and activity. Journal of Clinical Endocrinology and Metabolism. 59(5):955-962, 1984.

Dorgan JF, JT Judd, C Longcope, et al. Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. American Journal of Clinical Nutrition. 64(6): 850-5, 1996 Dec.

Field AE, GA Colditz, WC Wilett, et al. The relation of smoking, age, relative weight, and dietary intakes to serum adrenal steroids, sex hormones, and sex hormone binding globulin in middle-aged men. Journal of Clinical Endocrinology and Metabolism. 79(5):1310-1316, 1994.

Hamalainen E, H Adlercreutz, P Puska, et al. Diet and serum sex hormones in healthy men. Journal of Steroid Biochemistry. 20(1): 459-464, 1984 Jan.

Hill PB & EL Wynder. Effect of a vegetable diet and dexamethasone on plasma prolactin, testosterone, and dehydroepiandrosterone in men and women. Cancer Letters, 7:273-282, 1979.

Hill PB, EL Wynder, L Garbaczewski, et al. Diet and urinary steroids in black and white North American and black South African men. Cancer Research. 39:5101-5105, 1979.

Hill PB, EL Wynder, L Garbaczewski, et al. Plasma hormones and lipids in men at different risk for coronary heart disease. American Journal of Clinical Nutrition. 33: 1010-1018, 1980 May.

Howie BJ & TD Shultz. Dietary and hormonal vegetarian Seventh-Day Adventists and nonvegetarian men. American Journal of Clinical Nutrition. 42: 127-134, 1985 July.

Key TJA, L Roe, M Thorogood, et al. British Journal of Nutrition. 64:111-119, 1990.

Meikle AW, JD Stringham, MG Woodward, et al. Effects of a fat-containing meal on sex hormones in men. Metabolism: Clinical & Experimental. 39(9): 943-946, 1990 Sep.

Raben A, B Kiens, EA Richter, et al. Serum sex hormones and endurance performance after a lacto-ovo vegetarian and a mixed diet. Medicine & Science in Sports & Exercise. 24(11): 1290-1297, 1992 Nov.

Reed MJ, RW Cheng, M Simmonds, et al. Dietary lipids: an additional regulator of plasma levels of sex hormone binding globulin. Journal of Clinical Endocrinology & Metabolism. 64(5): 1083-5, 1987 May.

Rosenthal MB, RJ Barnard, DP Rose, et al. Effects of a high complex carbohydrate, low-fat, low-cholesterol diet on levels of serum lipids and estradiol. American Journal of Medicine. 78(1): 23-27, 1985 Jan.

Tsai L, J Karpakka, C Aginger, et al. Basal concentrations of anabolic and catabolic hormones in relation to endurance exercise after short-term changes in diet. European Journal of Applied Physiology & Occupational Physiology. 66(4): 304-308, 1993.

Volek JS, WJ Kraemer, JA Bush, et al. Testosterone and cortisol in relationship to dietary nutrients and resistance

[Emma-Leigh]

I need cliffs Mike please speed this up
- What is the actual "minimum required" daily fat intake level before stuff goes wrong?
- Is going as high as 0.35-0.5g/lb of fat per day really necessary, even if overall caloric intake is low enough that this leaves not much room for carbs (50g or so)?
- Re: more (unsaturated) fat being better for glucose metabolism - is this also relevant to folks like us who are aware of how glycemic levels change in response to a meal? We can also lower the glycemic response by eating more fiber or lower-GI carbs in general. This seems like a more useful guideline for the average guy eating too many refined carbs and who doesn't want to think about it.
- Re: more fat being better for test production - does this actually make a relevant difference on performance, body composition, etc? Jamie Hale has an article on how even among the drugged population, there's a "minimum threshold dose" of test you need to get to even see any difference. He uses this argument to assert that this is why test boosters are useless - even if they raise test levels it usually isn't enough for that to actually do anything. In light of this, is dietary fat's effect on test here really that extreme?

Any insight would be appreciated.

Sincerely,
#1 bro

First ->> this turned up in my e-mail and I thought of you (have full text if you are interested):

ANNUAL BNF LECTURE
The role of fat in the diet – quantity, quality and sustainability
nbu_1824 138..146
T. A. B. Sanders
King’s College London, UK

Summary
Dietary fat should supply at least 15% of food energy including 2.5% energy and 0.5% energy as linoleic acid and alpha-linolenic acid respectively: docosahexaenoic acid may also need to be supplied in infants. The proportion of energy from fat is not linked to risk of obesity, cardiovascular disease and cancer. The total cholesterol/HDL cholesterol, which is the most robust lipid indicator of risk of coronary heart disease (CHD), is lowered by unsaturated fatty acids, increased by trans fatty acids and not affected by saturated fatty acids compared with carbohydrates. Using clinical outcomes as endpoints, trans fatty acids increase, polyunsaturated fatty acids decrease and monounsaturated and saturated fatty acids have no effect on CHD risk. Recent recommendations for the prevention of CHD suggest partial replacement of saturated with polyunsaturated fatty acids to give energy intakes in the range of 6–11% energy and a daily intake of 0.25 g long-chain n-3
polyunsaturated fatty acids. The recommendation to increase the intake of longchain n-3 fatty acids needs to be considered against the backdrop of falling fish stocks; it is likely that a novel source will be needed in the future. The projected growth in world population will require more fat, mainly for food energy. The oil palm requires only one tenth of the land required by oil seeds to produce the same amount of oil. The impact of increased use of vegetable oils as biodiesel needs to be urgently reconsidered owing to the adverse environmental and economic consequences to people living in South East Asia.
Keywords: cardiovascular disease, dietary fat, essential fatty acids, obesity, sustainability

But to go back to your questions:
- What is the actual "minimum required" daily fat intake level before stuff goes wrong?
^ see above quote... but I have quoted before the average person should aim for about:

This is very hard to say - it depends on many things such as a persons age, or stage in growth and development (or if they are pregnant/ breastfeeding in the case of a female), their training status, and if they have any underlying health concerns or goals.

Omega-6 fats (Of which I would consider LA 'essential') are usually found at sufficient levels in most peoples diets, but something around 10-20g a day (being slightly less in females/ more in males) is 'an adequate minimum' for most people (male and female) between 18 and 45 to 50 years. In terms of % of diet - most suggest about 4-6% coming from omega-6 fats.

Omega-3 fats (of which I would consider ALA, EPA and DHA all 'essential' due to the poor conversion rates) needs to be, at a minimum, a combined total about 6-7g (once again - range of between 5 and 10g). So that is about 2-4g of ALA, and a combined total of 2-3g of EPA and DHA (eg: 6 to 10g fish oil caps a day).

To combine them - it would be a 'minimum healthy % PUFA fat' of about 8-10%

But, once again - I restate that these are MINIMUMS for 'health'. They are not what is 'optimal' nor 'best', especially for those who are in heavy training or have other issues to consider.


- Is going as high as 0.35-0.5g/lb of fat per day really necessary, even if overall caloric intake is low enough that this leaves not much room for carbs (50g or so)?
depends... but for SHORT durations - if you can withstand the hormonal and hunger issues associated with very low fat diets - it is fine to go lower.


- Re: more (unsaturated) fat being better for glucose metabolism - is this also relevant to folks like us who are aware of how glycemic levels change in response to a meal? We can also lower the glycemic response by eating more fiber or lower-GI carbs in general. This seems like a more useful guideline for the average guy eating too many refined carbs and who doesn't want to think about it.
Yes and no. Can you achieve some glucose control benefits from combining higher fiber/ lower glucose load carbs with protein etc.... Yes. Does that mean that using unsaturated fats will not help over and above this? No.

Additionally - unsaturated fats have other benefits over and above glucose control - eg: cholesterol, blood pressure, vascular health, anti-inflammatory etc etc.


- Re: more fat being better for test production - does this actually make a relevant difference on performance, body composition, etc? Jamie Hale has an article on how even among the drugged population, there's a "minimum threshold dose" of test you need to get to even see any difference. He uses this argument to assert that this is why test boosters are useless - even if they raise test levels it usually isn't enough for that to actually do anything. In light of this, is dietary fat's effect on test here really that extreme?
Basically:
Very Low Fat eventually -> lack of test. (as can low calorie / excess exercise/ etc etc)....
More fat over and above that which is minimally required -> will not significantly 'enhance' testosterone over and above normal levels.

[Insight]

First ->> this turned up in my e-mail and I thought of you (have full text if you are interested):

Wow. yes please. So they're saying that sat fats have an equally negative impact on HDL/LDL ratios as do carbs? Might this have something to do with the fact that saturated fats are typically more insulinogenic than PUFAs, and that cholesterol metabolism being screwed up was shown to be positively correlated with insulin resistance in that other study?


- Is going as high as 0.35-0.5g/lb of fat per day really necessary, even if overall caloric intake is low enough that this leaves not much room for carbs (50g or so)?
depends... but for SHORT durations - if you can withstand the hormonal and hunger issues associated with very low fat diets - it is fine to go lower.

All I know is that I feel worse on less carbs and more fats. And beyond that, most of the bodybuilding world is on this "carbs in the morning, fat in the evening" schedule, but I feel better on the opposite - more fat in the morning (gives me more stable energy levels throughout the day) and more carbs in the evening (I have no idea why). But hunger issues for me are generally more with low carbs. Maybe this means I'm more insulin sensitive...?


Basically:
Very Low Fat eventually -> lack of test. (as can low calorie / excess exercise/ etc etc)....
More fat over and above that which is minimally required -> will not significantly 'enhance' testosterone over and above normal levels.

Do you know any numbers for what is required to keep test levels up? Or is it just the numbers you wrote above, the ~27g of PUFA a day?

[NorCALSpeed]

It figures that the best thread that pops up on my quest for fat knowledge-and it's affect on T levels- while cutting would involve Insight. My old "Losing fat for Newbs" buddy.

I am very interested in learning about this as well. I've been cutting for several months, and I know my T levels are down, due to a lowered sex drive. I also have decreased energy. I've been opting for a lower fat, higher carb diet because like Insight, it keeps me feeling full and happy. Food satiation for me is a lot about volume. I find a higher carb meal keeps me happy through the day, rather than a high fat, low carb meal. It's so hard to find the balance when you're cutting, it seems like you just have to pick low carbs or low fats, because keeping them at "optimal levels" means quickly passing your proper deficit.

I certainly don't want to do a keto diet, but perhaps carb-cycling (even though it goes against wave length) is the way to balance the carb cravings and fats needed? A day of high fat, low carb followed by the opposite.

Insight, I'm eating at the same calorie amount as you. Generally my macros break up to 160gP (640 cals), 35g Fat (315 cals) and 125g Carbs (the rest, 500ish). Is this about what your daily goals are?

It was hard to decipher those studies (maybe my brain is running slow because of a lack of fats? Ha!) but it looks like we need at LEAST 30g a day?

[Trillios]

Wow. yes please. So they're saying that sat fats have an equally negative impact on HDL/LDL ratios as do carbs? Might this have something to do with the fact that saturated fats are typically more insulinogenic than PUFAs, and that cholesterol metabolism being screwed up was shown to be positively correlated with insulin resistance in that other study?



All I know is that I feel worse on less carbs and more fats. And beyond that, most of the bodybuilding world is on this "carbs in the morning, fat in the evening" schedule, but I feel better on the opposite - more fat in the morning (gives me more stable energy levels throughout the day) and more carbs in the evening (I have no idea why). But hunger issues for me are generally more with low carbs. Maybe this means I'm more insulin sensitive...?



Do you know any numbers for what is required to keep test levels up? Or is it just the numbers you wrote above, the ~27g of PUFA a day?

BUMP. Would also like to know the answers if possible.