The Balanced Macro Diet

When you first begin training, it becomes almost immediately apparent that you will need to eat well if you’re going to reach your goals. But how much protein should you be eating each day? Should you be eating high carb and low fat? Some say that you should be eating twice as many calories from carbohydrates as protein. Others suggest a more balanced ratio. What worked for me was to start by consuming the same amount of calories from each macronutrient. This formula will get many of you pretty damn far.

How many total calories will you need each day to support your metabolism and fuel the addition of new muscle tissue? Don’t worry because I am going to make it incredibly simple for you. Follow the easy steps outlined below and you will be on your way to a sensible, balanced diet that will help you get started…and then some. All you need to know is your body weight.

 

Read the full article by Evan Centopani @animal

Organ Meats: Wild predators eat these juicy bits first, and so should you. Well, at least occasionally. Here’s why.

 

tip-eat-gross-organ-meats

 
For those who grew up eating traditional Western diets, the thought of eating kidneys or intestines can be cringe inducing. But organ meats have always been the preferred animal protein source for hunters across a wide range of cultures. In fact, even in the animal kingdom most predators go after organs first (namely the liver) before eating the more muscular cuts. What is it that these predators know about organ meats that most people don’t?

The Secret is Nutrient Density

Organ meats are some of the most nutrient dense foods on the planet. They’re quality protein sources that are also rich in essential fatty acids, vitamins, and minerals. When classifying the nutrient density of food (nutrients per serving divided by weight), organ meats top the list.

Compare 4 ounces of beef liver with 4 ounces of chicken breast (without skin). While the liver and chicken have pretty similar levels of protein and essential amino acids, the liver blows chicken breast out of the water when you look at the vitamin and mineral content.

The Best Bits

Liver

This can be eaten raw or cooked and can be prepared in a variety of ways: jerky, part of a pate, or ground up with other meat in burgers or meatballs. Liver is also a good source of vitamin A, all of the B vitamins, vitamin C, iron, phosphorous, selenium, copper, manganese, and zinc.

Vitamin A plays a role in immune function through the development of both t-cells and b-cells. Manganese plays a role in the metabolism of carbs, amino acids, and cholesterol. Zinc supplementation has been shown to augment the effects that exhaustive exercise has of decreasing thyroid and testosterone levels. In studies, the participants that supplemented with zinc had higher hormone values after four weeks.

Common sources: Beef, lamb, buffalo, chicken, turkey, duck, geese.

Heart

Since the heart is a tough muscle, it eats more like a steak or a roast. Heart can be grilled, charbroiled, or marinated. It’s a good source of B vitamins, iron, selenium, phosphorus, copper, and CoQ10.

B vitamins play a role in cellular energy production, red blood cell formation, and the metabolism of amino acids, glycogen, and fatty acid synthesis. Copper helps with iron absorption and thyroid function. Iron is necessary for oxygen transport and plays a role in cellular energy production.

CoQ10 is an antioxidant that can reduce lipid perioxidation, lower blood pressure, and increase blood flow. Another additional benefit is that when used by the body, CoQ10 becomes reduced to a compound known as ubiquinol. Studies have shown that ubiquinol can significantly improve maximum power output.

Common sources: Lamb, pork, beef, chicken.

Kidneys

Grill them or mix them with sauces or as part of a stir fry. Kidneys are a good source of B vitamins, iron, phosphorus, copper, selenium, zinc, and vitamin C.

Phosphorus deficiencies have been linked to muscular fatigue. Selenium offers neuroprotective benefits, is required for the synthesis and metabolism of thyroid hormones, and has been shown in studies to increase testosterone levels with as little as 200 mcg.

Common sources: Beef, lamb, pig, goat.

Tongue

One of the most tender cuts of meat because of its fat content, it can be stewed, pickled, slow-cooked, or poached. Tongue is a good source of zinc, potassium, B vitamins, choline, and monounsaturated fatty acids.

Choline plays a variety of roles in the body including cell structure and neurotransmitter synthesis. Potassium regulates fluid balance and plays a role in controlling the electrical activity of the heart and muscles.

Common sources: Beef, pork, goat, lamb.

organ-meat

Wait! But What About…

High cholesterol and saturated fat content?

For years, nutritionists, doctors, and other health experts have hammered away about the dangers of cholesterol. Well, in a 15 year study researchers followed over 12,000 adults and discovered that the groups with total cholesterol levels below 160 mg/dl and above 240 mg/dl were most at risk for cardiovascular diseases. The distribution of hazard ratios followed a U-shaped curve. Consumed in moderation, saturated fats and cholesterol are beneficial for the roles they play in regulating hormonal balance, production of vitamin D3, neural signaling, and immune function.

Toxicity?

Yes, the liver and kidneys act as filters. But it’s important to remember that while these organs function as filters, their jobs are to excrete toxins from the body, not store it. If it’s still a concern, just choose younger animals that have less exposure to pesticides and other toxins (like veal over beef) or opt for grass-fed animal products.

Taste?

It’s subjective. Our tastes are shaped by a combination of personal preference and sensitivities to certain flavors, and exposure to these foods. Some people rave about the unique flavor of organ meats; others say they’re acquired tastes, and others flat-out dislike them. Ease your way in by starting out with muscular cuts (heart, tongue) that are closer in flavor and texture to typically consumed cuts of meat, then transition to choices like liver and kidneys that have more distinctive flavors.

Where to Get Organ Meat

Another name for organ meat is offal. It’s become easier to find at most grocery stores due to the popularity of “nose to tail” eating. If your local chain isn’t up to speed, check out the specialty ethnic stores in your area.

References

  1. Kilic, M. (2007). Effect of fatiguing bicycle exercise on thyroid hormone and testosterone levels in sedentary males supplemented with oral zinc. Neuro Endocrinology Letters, 28(5), 681-685.
  2. Kil, M., Baltaci, A., Gunay, M., Okudan, N., & Cicioglu, I. (2006). The effect of exhaustion exercise on thyroid hormones and testosterone levels of elite athletes receiving oral zinc. Neuro Endocrinology Letters, 27(1), 2nd ser., 247-252.
  3. Alf, D., Schmidt, M. E., & Siebrecht, S. C. (2013). Ubiquinol supplementation enhances peak power production in trained athletes: A double-blind, placebo controlled study. J Int Soc Sports Nutr Journal of the International Society of Sports Nutrition, 10(1), 24.
  4. Safarinejad, M. R., & Safarinejad, S. (2009). Efficacy of Selenium and/or N-Acetyl-Cysteine for Improving Semen Parameters in Infertile Men: A Double-Blind, Placebo Controlled, Randomized Study. The Journal of Urology, 181(2), 741-751.
  5. Bae, J., Yang, Y., Li, Z., & Ahn, Y. (2012). Low Cholesterol is Associated with Mortality from Cardiovascular Diseases: A Dynamic Cohort Study in Korean Adults. Journal of Korean Medical Science J Korean Med Sci, 27(1), 58.

Neuroscience Reveals What Fasting Does To The Brain (And Why Big Pharma and the Food Industry Won’t Study It)

I came across this TEDx talk given by Mark Mattson, the current Chief of the Laboratory of Neuroscience at the National Institute on Aging. It presents some fascinating details about fasting and why it isn’t as popular as it should be.

Many research studies are showing its benefits. This article by Authority Nutrition highlights 10 evidence-based health benefits of fasting that studies have found. These include weight loss, lower blood pressure and reduced cholesterol.

But the real interesting question is, why won’t the pharmaceutical industry study it?

Here is a transcript of a section of Mark Mattson’s talk which hints at these questions:

“Why is it that the normal diet is three meals a day plus snacks? It isn’t that it’s the healthiest eating pattern, now that’s my opinion but I think there is a lot of evidence to support that. There are a lot of pressures to have that eating pattern, there’s a lot of money involved. The food industry — are they going to make money from skipping breakfast like I did today? No, they’re going to lose money. If people fast, the food industry loses money. What about the pharmaceutical industries? What if people do some intermittent fasting, exercise periodically and are very healthy, is the pharmaceutical industry going to make any money on healthy people?”

Please watch and share so we can raise questions about our eating habits and how we can become more healthy.

To further back up the benefits of fasting, here is a quote from an author from The Power of Ideas who tried intermittent fasting for one month:

“Intermittent fasting has now become my way of life. It feels damn good and I find myself being clear and focused. My energy levels have sky rocketed. I used to always get that afternoon slump when I felt tired at about 3 PM, but I don’t experience this anymore.

Eating has also come to be an experience that’s enjoyed, rather than just food to scoff down as fast as I can. This has made it easy to keep intermittent fasting going.

Also, after a couple weeks, I decided to try exercising (running and weights) as soon as I woke up on an empty stomach. I thought I would feel light headed and faint from working out on an empty stomach, but the truth is, I had more grit and energy.

Research has found that there’s major perks to doing this: apparently it’s meant to supercharge your body’s fat-burning potential.”

Gut Health Inflammation and Mood Disorders

Evidence is making it very clear that there is a strong association between gut health, brain function and mood.

brain-gut-connection

It has long been known that stress can wreak havoc with our digestive tract. It appears now that problems in the GI tract can also negatively impact the brain. Potentially causing anxiety and depression.

In other words, what is transpiring in your gut may directly influence central nervous system function. Hence gut health influences neural circuitry and can therefore have an effect (positive or negative) on behavior.

The newest research suggests, for instance, that how your digestive tract evolves in the first few years of life can influence the health of your brain. This also means it will subsequently affect your behavior in the future. This hypothesis is predicated upon the way in which a healthy GI floral population positively influences neurons involved in motor control and behavior. In the case of those with overwhelming populations of gut pathogens or gut dysbiosis, it can pave the way for the development of anxiety and depression later in life.

Microbiota, Inflammation, Autoimmunity, Depression

Gut health and gastrointestinal compromise can be a mechanism for the origins of systemic inflammation and autoimmunity. Since both inflammation and autoimmune conditions have also been associated with the genesis of mood disorders. It is only reasonable to suggest, again, that an intimate relationship between gut health, brain function and mental health exists. As one recent study demonstrates, inflammatory bowel disease in animal experiments can have an adverse effect on the hypothalamus. It does so by increasing the sensitivity of the HPA axis to stress.

Regarding the inflammatory process and depression, one study took interest in new moms. It went as far as to suggest that addressing inflammation in new moms could possibly go a long way in helping to prevent the symptoms of postpartum depression. Another study suggested a cause and effect relationship between GI inflammatory/intestinal permeability and the pathogenesis of alcoholism.

As some of the previous studies have established, it appears quite irrefutable that there is constant communication between our microbial symbiotic gut inhabitants and ourselves. In this case it is more precisely between our central nervous system through GABA receptors in the vagus nerve.

Probiotics

Taking this discussion a step further, could it be that certain human strains of probiotics have a therapeutic effect? Could they positively influence mood? Could we further emphasize this special symbiotic relationship? Several studies have shown that this is indeed the case.

One particular strain, Bifidobacterium infantis, was shown to significantly influence the stress response. It does so by normalizing specific measurements of the HPA axis. It also improves the immune response and cytokine modulation. So, this particular strain offers an interesting modulation of stress and depression.

Researchers continue to find evidence to support the opinion that the brain can directly communicate with the microbiota. These diverse bacterial populations make up the natural environment of the GI tract. In fact, the microbiota has intimate control of the function of the GI tract through the vagus nerve. According to one study, “Since the interactions of microbes with host lead to a complex balance of host genes, alteration of microbiota population can cause several metabolic disorders.”

This implies the importance of maintaining the health of the digestive system’s bacterial micro-environment. And makes the significance of probiotic use quite evident.

The relationship and communication between our gut and brain is profound and intimate. This knowledge further brings into focus the importance of maintaining an optimally functioning gastrointestinal tract. This also strengthens the view that perhaps the gastrointestinal system be a priority in the evaluation of new patients. Since if overlooked or taken for granted may lead us away from an important cause of many chronic diseases.

References:

1) The intestinal microbiota affect central levels of brain-derived neurotropic factor and behavior in mice. Gastroenterology, 2011 Aug;141(2):599-609, 609.e1-3. doi: 10.1053/j.gastro.2011.04.052. Epub 2011 Apr 30

2)  Transient Gastric Irritation in the Neonatal Rats Leads to Changes in Hypothalamic CRF Expression, Depression- and Anxiety-Like Behavior as Adults  PLOS ONEDOI: 10.1371/journal.pone.0019498

3)  A new paradigm for depression in new mothers: the central role of inflammation and how breastfeeding and anti-inflammatory treatments protect maternal mental health,International Breastfeeding Journal, 2007, 2 :6 doi:10.1186/1746-4358-2-6

4) Role of intestinal permeability and inflammation in the biological and behavioral control of alcohol-dependent subjects, Brain Behav Immun.,2012 Aug;26(6):911-8. doi: 10.1016/j.bbi.2012.04.001. Epub 2012 Apr 10

5) Effects of the probiotic Bifidobacterium infantis in the maternal separation model of depressionNeuroscience. 2010 Nov 10;170(4):1179-88. doi: 10.1016/j.neuroscience.2010.08.005. Epub 2010 Aug 6.

6) Gut-central nervous system axis is a target for nutritional therapies, Nutrition Journal 2012, 11:22  doi:10.1186/1475-2891-11-22

7) Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve, Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16050-5. doi: 10.1073/pnas.1102999108. Epub 2011 Aug 29

The Bulking Diet Delusion

DirtyBulk_BlogFeature

by John Meadows @t-nation.com/diet-fat-loss/bulking-diet-delusion

Here’s what you need to know…

  1. Bulking up by increasing body fat will decrease insulin sensitivity and impede muscle growth.
  2. The more fat you gain, the more you change your physiology to favor fat storage over muscle growth.
  3. Most people who bulk will store fat in just one area, like the belly or love handles, making it tougher and tougher to lean that area out.
  4. Bulk up too much and your muscles will get softer due to ectopic fat storage. The body will store excess calories, not just as adipose, but in muscle tissue as well.
  5. Repeatedly gaining fat in the off season and then having to lose it all will lead to metabolic damage and stubborn fat storage.
  6. You need a caloric surplus to build muscle, but gaining five pounds of fat in order to gain one pound of muscle is a bad idea.

Scale Weight: The Old Barometer for Bulking Success

The rules of off-season bulking used to be simple: Eat every two to three hours and eat until full. While “clean” foods like chicken and brown rice were the ideal, no one was docked points for sneaking in a pizza during the post-workout “window of opportunity.”

As long as the number on the scale was growing, that was all that mattered. Scale weight became the metric by which you judged the success of a bulk.

It usually wasn’t a pretty process. Let’s say you decided to bulk up to 250 pounds by Christmas. Pants getting tight at 235? Get stretchier pants. Can’t fit into your suits at 240? Make every day casual Friday!

The idea was to just keep eating. When the scale says 250 pounds, you win.

But did you really win? You gained 30 to 50 pounds in four or five months. You might have a bigger bench and squat. You might also have chipmunk cheeks and a low back that barks even when you do a single rep of tying your shoelaces.

But are you any better after an all out bulk? No. There are seven reasons why:

1 – Muscle Growth is Slow

Building muscle – actual, contractile muscle tissue – is a painstakingly slow process for any lifter past the beginner phase.

For an experienced lifter, a gain of 1-2 pounds a month of pure muscle would be excellent. It adds up to 10 pounds or more in a single off-season. However, only a scant few bodybuilders can gain muscle at such a rate, and 10 pounds is a far cry from the 40 or 50 pounds you slapped on during your bulk.

 

2 – Insulin Sensitivity Decreases

When you bulk up and body fat levels rise, you can gradually decrease insulin sensitivity, which can impede muscle growth. Insulin is actually a signaling protein for both muscle and fat cells to utilize amino acids and glucose.

Ideally, insulin-sensitive muscle cells will readily absorb glucose and amino acids when insulin “signals” them to open. With increased body fat, though, comes increased levels of insulin, and this can desensitize muscle cells to insulin’s signaling effects.

If you decrease insulin sensitivity, your muscle won’t use glucose and amino acids as efficiently, and since it’s metabolically less expensive to store fat, your body will convert more of the excess calories into body fat.

The more overweight you are, the more you change your physiology to favor fat storage over muscle recovery and growth.

 

3 – You Build Anabolic Resistance

This physiological phenomenon where protein synthesis is inhibited and fat storage is elevated is referred to as anabolic resistance, and it’s the last thing you want as a bodybuilder.

The fatter you get, the more likely it is that any excess nutrients you eat are being stored in your butt and gut – not your quads and biceps. And, the less likely it is that your training is leading to any actual muscle growth.

Of course, there are always outliers. I know guys who can gain 50 pounds in an off-season and just get bigger all around. Exceptions don’t make rules however, and simply because the top guys can “get away” with a bulking strategy doesn’t make it a sound option for the majority of us who are less genetically gifted.

 

4 – Brand New Fat Cells, Accelerated Fat Storage

Past a certain body fat point, you’re simply accelerating fat storage. The average bulker will store most of his fat in just one unsightly area, like the belly or love handles.

Not only is this unhealthy (fat around the abdomen is directly correlated with heart disease and hypertension), it can lead to the creation of new fat cells that make it even harder to diet down once bulking ends. This process is called adipogenesis, and it occurs during periods of intense weight gain and caloric surplus.

When someone is doing heavy-duty bulking, the excess calories all get eventually converted to glucose, which is essentially sugar. Glucose gets used by both muscle and fat cells for energy usage and storage.

But when glucose levels are continuously high, and you have more than you need for just your muscles, all that excess glucose will be stored as fat. This is why hard and fast “dirty” bulking rarely leads to large increases in muscle.

Over time, as bulking is repeated, you’re actually fattening up the same parts of your body. This makes for a total bitch of a diet. If it’s already hard to whittle away at that one area, adding even more fat there means you should prepare for 12 weeks of hell.

Even worse, the higher your body fat levels climb, the greater the possibility of it leading to anabolic resistance. Getting that stubborn area down will likely hurt other areas too, and actually make them appear emaciated. Consequently, it can negate any muscle gains.

 

5 – Softening Muscles

Ectopic fat storage makes matters worse. Because the body is being flooded with excess calories, glucose, and triglycerides, it’ll begin storing the excess not just in adipose tissue, but in the muscles themselves.

This is called intramuscular triglyceride storage. This contributes to dirty bulkers who get a soft appearance to their muscles.

It’s not just cosmetic, though. Intramuscular fat can also inhibit protein synthesis and subsequent muscle growth.

You’ve likely seen the occasional bodybuilder who got huge in the off-season but somehow lost all his soft gains when he dieted back down. Ectopic fat storage is only partially responsible for that happening.

 

6 – Sluggish Metabolism

Getting fat over and over again can make getting leaner more difficult each time.

If you get too fat and then have to kill yourself to diet down, the body will hang onto fat that much harder the next time you diet.

This particular phenomenon is somewhat related to the metabolic damage concept of reducing basal metabolism over and over again to the point where weight loss is nearly impossible and weight gain can be caused by even the slightest of calorie surpluses.

While metabolic damage is often associated with female competitors, male bodybuilders can experience the same effects, but to a very different degree.

Picture a male bodybuilder that bulks up to 300 pounds in the off season but has to diet down to 250 on stage. That’s a 17% reduction in weight. Basal metabolism will begin to drop whenever there’s a 10% reduction in weight, so this bodybuilder is going to be slowing his metabolism as he diets.

If, however, he dirty bulked, he probably has to deal with anabolic resistance, too. If he repeats the dirty bulking process again post-contest, he’s reinforcing the increased fat storage and anabolic resistance that he experienced before.

This will make it harder for him to lean down for each contest, and each time he bulks up he’ll be less and less likely to put on any new muscle. He might not be experiencing metabolic damage in the classical sense, but metabolically he’s causing a lot of things to go wrong.

 

7 – You Probably Can’t Get Away With It

What the absolute top guys do is often the result of what they can get away with because of their genetics and drug use. It’s not necessarily a model for everyone else to follow. If you want competitive longevity, consider a more conservative approach.

Bodybuilders have bulked up and cut down for decades. This includes more than a few Mr. Olympia winners. It would be silly to say the approach doesn’t work because it clearly has.

But what you don’t hear about are the thousands of guys who bulked up, got too fat, messed up their insulin sensitivity, and never reached their true potential in either size or conditioning.

Consider also the guys that started out with a bang and looked amazing in one or two shows, but were never able to repeat that level of conditioning or fullness again.

 

Knowing When to Stop

The decision to bulk or not boils down to knowing your body. You need a calorie surplus to build muscle, and it’s hard to eat just enough to build muscle without some fat gain. But gaining five pounds of fat to gain one pound of muscle is a bad idea.

You’re more likely to lose that pound of muscle because of trying to diet that five pounds of fat off.

There’s no reason for most guys to get above 12% body fat. Personally, I prefer to stay under 10%. It will depend on where you start to lose insulin sensitivity – you’ll know you’re there as pumps will decrease and your muscles will start looking soft. If that happens, take it as a sign to end your bulk.

Foods to Boost DHT Levels and 5-Alpha Reductase Naturally

Dihydrotestosterone (DHT) is a controversial hormone. Even though it’s the male hormone of the male hormones and a lot more androgenic than testosterone, some are still scared that high levels of it could lead to hair-loss and prostate enlargement.

Whereas the prostate claim has proven to be inaccurate in multiple studies (for example: in this study, 10-fold increase in serum DHT levels had no significant effects on prostate size), the hair loss side-effect of DHT still remains partially unclear (even though in this study with 315 male subjects, it was noted that high DHT levels were associated with a -35% reduced risk of hair loss).

I’m not going to dig deeper into the subject of possible DHT side-effects in this post, since a bunch of men who already seem to understand the importance of having high DHT (amen brothers), have been asking for me to write more about the subject of boosting the king of androgens via good nutrition…

…And that’s exactly what we’re covering here today. How to squeeze out more DHT from your everyday diet.

 

1. Eat The Right Kinds of Fats

cheese-all

Dietary fat is one of the most important factors in healthy testosterone production, and not that surprisingly, also in dihydrotestosterone production.

This is because the increased intake of dietary fat boosts testosterone levels, and about 5-15% of that testosterone eventually converts into DHT by the actions of the 5-alpha reductase enzyme.

Eating more dietary fat will also increase the levels of the 5-a enzyme needed for that conversion, so don’t forget to eat your damn fats.

I generally recommend about 25-35% of daily calories from fat in order to raise T and DHT levels. However, what’s more important than the amount of the fats, is the type of them…

…Because when it comes down to DHT boosting fatty-acids, all of them are definitely not created equal:

Different Types of Dietary Fat and DHT:

a) It’s a well known fact that PUFAs, aka. polyunsaturated fatty-acids (especially the rancid ones from processed vegetable oils) lower testosterone levels, and therefore also DHT levels. PUFAs also directly inhibit the formation of 5-alpha reductase enzyme in the following inhibitory potency: Gamma-linolenic acid -> Alpha-Linolenic acid -> Linoleic-acid -> Palmitoleic-acid -> Oleic-acid -> Myristoleic-acid.b) Saturated fatty-acids (SFAs) and monounsaturated fatty-acids (MUFAs) on the other hand seem to increase testosterone and DHT levels (study, study, study, study). However, certain saturated fatty acids can have a slight inhibitory effect on the 5-a reductase enzyme, at least if you believe this test-tube study where medium-chain fatty-acids (those commonly found in tropical oils such as: coconut and palm oil) reduced 5-a activity.

NOTE: That above study is not strong enough evidence for me to stop using coconut oil, since it has such beneficial effects on thyroid function, but if your only goal is to get high DHT, then perhaps don’t go crazy with the stuff.

Boosting DHT levels with dietary fat is very similar to that of testosterone. Just eat a lot of saturated and monounsaturated fatty-acids, while keeping your PUFA intake low. Also, if your goal is to maximize DHT production, then there’s some evidence that lowering the intake of medium-chain fatty-acids (coconut and palm oil) can be beneficial (but it’s not mandatory).

 

2. Eat More Carbs and Less Protein

20161004-baked-potato-vicky-wasik-10

This flies directly into the face of many fitness enthuasists and protein bros…

…you should eat less protein, more carbs. At least that is, if you want to maintain high testosterone and DHT levels.

There’s a lot of evidence showing that diets higher in carbohydrates and lower in protein are great for testosterone production (study, study, study)…

…And one study in particular which showed that a low-protein high-carb diet was superior in boosting DHT levels when compared to a high-protein low-carb diet, due to the fact that higher carbohydrate intake was associated with increased production of the 5-alpha reductase enzyme.

NOTE: If you’re looking to furthermore bump-up your DHT production via carbohydrates, thenconsider adding a grain by the name of sorghum to your diet, it increased 5-a enzyme levels by 54%.

I personally go by the carb to protein ratio of 3:1, and for me that is 60% carbs 20% protein. According to the study above, you could even go higher on carbs and lower on protein than the 2:1 example, but that could be detrimental for your gains in the gym.

 

3. Consider Organic Foods

healthy-organic-food

Organic foods may not taste that different than conventional produce, and they’re a hell of a lot more expensive too.

Hence, why a lot of people claim that it’s just a waste of money..

From a hormonal point of view, it’s definitely not a waste of money to eat organic though.

Several pesticides generously sprayed on conventional crops have shown to be strong anti-androgens that work by disrupting testosterone synthesis, DHT conversion, and 5-a reductase enzyme activity in the body (study, study, study).

I’m not saying that you have to completely stop eating conventional foods, but if you want to limit your exposure to anti-androgenic pesticides, then it’s not a bad idea to invest a bit on the quality of the stuff that goes into your mouth.

 

4. Drink More Coffee and Less Tea

coffee-beans-0-1920x434
I have great news for all you coffee fanatics, and some rather bad ones for tea lovers.

First of, the bad news: green tea catechins, at least according to this animal study, have 5-a enzyme inhibiting effects…

…Even worse, in this rodent study, theaflavins from black tea lowered DHT levels by -72% and 5-a enzyme levels by -89%.

Then for the good news: Caffeine has the opposite effect, it has increased testosterone levels in few human studies, and in this rodent study, caffeine increased testosterone by 68% and DHT by 57%. According to another study, caffeine acts as a catalyst to the 5-alpha reductase enzyme.

Relying on the evidence above, more coffee and less tea = more DHT.

 

5. Avoid Soy and Other Phytoestrogens

soy1
It’s a well known fact that phytoestrogen consumption increases estrogen levels, reduces testosterone levels, and has a negative impact on DHT conversion through the already lowered T, and also because many phytoestrogens act as 5-a inhibitors.

Therefore consuming high amounts of foods and drinks that contain phytoestrogens, such as: hops, flax, licorice, soy, etc, can easily become detrimental to your DHT levels.

The phytoestrogenic isoflavones (genistein, daidzein and glyciteinin) in soy are likely the worst offenders when it comes to DHT, since this study shows that men who consume a lot of these soy isoflavones (and also green tea!), produce high amounts of equol in their gut. Another study from 2004 shows that equol is a strong anti-androgen that binds and sequesters DHT from its receptor, rendering the androgen inactive.

Few other studies have shown that soy can reduce DHT (study, study).

So, to keep your DHT levels high and the receptor sites active, maybe cut down on the phytoestrogen consumption.

Source@ https://www.anabolicmen.com/section/nutrition/

Anabolic Resistance

How Mass Diets Can Hurt You

09/23/13
Anabolic-resistance

Here’s what you need to know…

  1. Anabolic resistance is the impaired ability to build muscle caused by excess calorie consumption over time.
  2. Eating more calories to build muscle is necessary, but there’s a point of diminishing returns. You may reach “nutrient overload” where fatty acids, triglycerides, and glucose become toxic.
  3. Insulin resistance is the first step toward anabolic resistance. You don’t have to be fat to develop insulin resistance. Anyone continually eating too much can develop insulin resistance in a few weeks.
  4. To fix anabolic resistance, reduce calories just below maintenance for a few weeks and decrease carb intake. Try to prevent inflammation as much as possible.

Bulking Gone Bad

You’ve dieted hard for months and got completely shredded. Although you’re in great condition, you also lost some size. Now the diet is over and you’re fired up to do some big eating. This year, you tell yourself, you’ll be bigger than ever.

You start to eat big to get big. You take in a huge surplus of calories and train like an animal. Over the next several weeks, all is well: strength is up, you’re getting unbelievable pumps in the gym, and you’re hungry all the time. This is what “anabolic” feels like. You know you’re growing.

After some time, things start to change, however. You’re starting to look a little softer as the body fat starts to accumulate. That full and muscular look you had starts to fade. You’re increasingly soft and bloated, your abs are fading, and manatees start to look at you amorously.

Fast forward several more weeks. Strength gains are less impressive, those legendary pumps are gone, and your joints and your body in general are starting to ache, a sign of chronic, low-grade inflammation.

What went wrong? The simple answer is that the fat-gain caused by your bulk induced a state of anabolic resistance. Yes, a surplus of calories is needed to fuel new muscle growth, but a calorie surplus is only helpful up to a certain point, after which excess fatty acids, triglycerides, and glucose become toxic.

At that point, you’re in “nutrient overload” and you’ve reached the point of diminishing returns. Many lifters have experienced this when in bulking mode.

Taken to the extreme, the same metabolic changes that limit muscle growth during periods of nutrient overload are also causes of metabolic syndrome, diabetes, and cardiovascular disease.

This isn’t to say that you’re in danger of becoming morbidly obese and diabetic the next time you decide to bulk. Those who train hard are metabolically resilient enough to avoid becoming diabetic when the calories go up for extended periods of time.

But, prolonged nutrient overload eventually causes negative metabolic adaptations that lead to varying degrees of anabolic resistance.

3 Steps to Anabolic Resistance

Diagram Anabolic Resistance

The reason muscle growth slows as body fat creeps up out of your optimal range is important to understand. Nutrient overload causes a cascade of negative effects that ultimately throw a metabolic wrench in the muscle growth process.

This is called anabolic resistance, which is the reduced ability to increase muscle protein synthesis in response to amino acids, mechanical loads, or other anabolic agents such as insulin or IFG-1.

Excess fat accumulation can make you more resistant to muscle growth even in the context of normal anabolic hormone levels. This is irrespective of insulin, IGF-1, or growth hormone availability.

Although training plateaus are inevitable, “metabolic plateaus” caused by misguided gluttony in an attempt to put on extra muscle are completely avoidable with smart nutrition. There are three factors associated with bulk-induced nutrient overload that lead to anabolic resistance.

Factor #1 — Insulin Resistance

Insulin resistance may be the most important, because it tends to be induced early-on.

You don’t need to be fat for several years to develop insulin resistance. Take any relatively young, healthy individual, put them in a state of nutrient overload, and insulin resistance will develop in a few weeks.

Insulin resistance increases the tendency to store carbs as fat, rather than packing them into muscle tissue as glycogen. It also causes the accumulation of triglycerides in muscle tissue, which contributes to muscle insulin resistance.

As muscle insulin sensitivity decreases, so does glucose uptake. The result is less stored glycogen, reduced muscle fullness, and less of a pump from training.

So bulking only works well – until you start to become less insulin sensitive. As body fat starts to accumulate of the optimal range, you become increasingly insulin resistant.

At this point, things start to go downhill fast, metabolically speaking. Fat stores expand, training progress slows, and it becomes difficult, if not impossible, to get a good pump in the gym.

Factor #2 — Leptin Resistance

Diagram Leptin Resistance

You’ve now reached the point of diminishing returns. As you become less insulin sensitive, you gain more and more fat. This is where leptin resistance comes in.

Leptin is a peptide hormone produced in fat cells (adipocytes) that functions as a controller of metabolism and as a hunger regulator. Technically speaking, it links changes in body fat stores to CNS control of energy homeostasis.

It helps to think of leptin as sort of a whole-body fuel gauge. Leptin monitors whole-body energy levels to coordinate energy expenditure, fat oxidation and overall metabolism.

As fat stores increase, adipocytes release more leptin into the circulation, which crosses the blood-brain barrier and communicates with leptin receptors in the hypothalamus.

This is a signal that you’re all “fueled up,” which triggers the hypothalamus to send signals to the brain and the rest of the body to decrease appetite and increase metabolic rate.

Likewise, when calorie intake decreases, fat cells produce less leptin. This tells the hypothalamus that fuel levels are low, triggering increased appetite and decreased energy expenditure. Leptin action isn’t just confined to just the hypothalamus, however.

There are leptin receptors all over the rest of the body, allowing leptin to globally coordinate appetite, metabolism, and energy expenditure.

As fat stores increasingly expand, more and more leptin is produced and released into the bloodstream. Eventually, when leptin levels are high enough for long enough, you develop leptin resistance. Leptin binds the leptin receptors, but no downstream messages are sent.

The fuel gauge is broken, and any fat-burning effects are lost. In spite of the extra body fat mass, the brain never gets the “fueled up” signal. As a result, you lose a degree of appetite control.

Certain people are more or less susceptible to this. The most fortunate of us become only slightly less insulin sensitive in response to prolonged bulking diets and may develop some degree of leptin resistance.

Those of us who have far-less resilient metabolisms with a pre-existing tendency to easily put on body fat have a much harder time; appetite control is broken, leading to continued fat gain.

This in turn causes more leptin resistance in the start of a vicious feed-forward cycle, bringing us to the final stage, where shit hits the fan, and you develop a full-on case of anabolic resistance.

Factor #3 — ER Stress – The Root Cause of Anabolic Resistance

ER stands for endoplasmic reticulum. Think of the ER as a protein factory.

The ER integrates metabolic signals to control glucose, lipid, and protein metabolism. It’s also a major site for protein synthesis. After being folded and processed in the ER, proteins are moved to the Golgi apparatus for further sorting, packaging, and distribution.

If the ER is the protein factory of your cells, then the Golgi apparatus is Fed-Ex. Proteins are then delivered from here to different parts of the cell.

Together, the ER and Golgi apparatus carry out the processing, transport, and delivery of all new proteins. The ER becomes stressed when demand for protein synthesis exceeds a cell’s ability to process, package, and ship new proteins out to their cellular destinations.

ER Stress In Adipose Tissue

Fat cells aren’t just passive storage containers for body fat. They also function as endocrine organs, secreting a number of different proteins to control metabolism, including leptin, adiponectin, and other peptide hormones. The larger a fat cell becomes, the more leptin it secretes, making the ER very important for fat cells.

It’s the job of the ER/Golgi apparatus to produce and process all that leptin. The system becomes overwhelmed when proteins are produced faster than they can be processed, resulting in ER stress.

This triggers the unfolded protein response (UPR), which reduces protein synthesis and increases ER protein folding capacity in an attempt to reduce the back-log of unprocessed proteins.

The problem is that this comes at a cost. UPR triggers an inflammatory response that can create a vicious cycle of inflammation and oxidative stress.

This “metabolic inflammation” is both a cause and an effect of ER stress. Nutrient excess causes an increased demand for protein synthesis in fat cells, both for the production of peptide hormones such as leptin, and for proteins needed for triglyceride production and fat storage.

When nutrient overload ramps up protein synthesis past ER’s ability to process/fold all these proteins, the UPR is triggered. All that protein synthesis is an energetically expensive process.

Insulin-resistant fat cells can’t take up enough glucose to meet the energy demands of protein synthesis. This triggers more ER stress. The result is a vicious cycle between inflammation, oxidative stress, insulin resistance, and leptin resistance.

ER Stress In Muscle Tissue

When nutrient overload triggers the ER stress response in fat cells, fatty acid uptake slows down. This causes some spillover into muscle tissue.

Insulin-resistant muscle tissue is ill-equipped to burn this fat for energy, so it gets stored as intramuscular triglyceride instead. This ectopic fat storage decreases insulin sensitivity in muscle tissue and also causes muscle ER stress, which is the root cause of anabolic resistance.

When the ER stress response is triggered in muscle tissue, you’re in a state of anabolic resistance. Muscle becomes less responsive to all the triggers for protein synthesis. Leucine uptake, mechanical loading, and even anabolic hormones become less effective at activating the protein synthesis machinery.

In short, nutrient overload is a cause of anabolic resistance. The fatter you get, the more insulin resistant you become. Insulin resistance is both a cause and an effect of leptin resistance, because it causes fat gain. When you’re in an insulin- and leptin- resistant state, you’re more susceptible to ER stress, the root-cause of anabolic resistance.

Two Tips to Avoid Anabolic Resistance

Tip #1 – Don’t get too fat.

Keep body fat within a certain range at all times. The ideal range is different for different people, depending on insulin sensitivity and other individual factors. If you exceed this range, you’ll know it.

More of the weight you put on will be fat, gains will slow down, the pump you get during training will be reduced, and you just won’t have that same degree of muscle fullness. It’s obviously best to avoid this in the first place by eating smart.

Tip #2 – Fix it.

To get better, pushing the limits is something we need to do. For this reason, it’s not uncommon to find yourself in a situation where you pushed it a bit too hard for too long with the calories, arriving at the point of diminishing returns. All is not lost.

The only way to move forward in this situation, however, is to go slightly backwards. Reduce calories to below maintenance levels for a few weeks and decrease carb intake. Add a little cardio if necessary.

When over-bulked, chronic, low-grade inflammation induced by nutrient overload may be a very real issue. Supplements like cyanidin 3-glucoside, curcumin, and fish oil are indispensible here to limit inflammation and promote insulin sensitivity.

Increased intake of food-based antioxidants or supplements like Superfood that are loaded with potent natural antioxidants may also help throw a wrench in nutrient-overload induced oxidative stress.

Continue the inflammation/oxidative stress-management and dieting phase until your body fat is back to an acceptable range.

You’ll then have cleared up any anabolic resistance and will be metabolically primed to continue packing on quality muscle. It’s not a coincidence that those who alter periods of increased calorie intake with dieting phases have physiques that just seem to evolve over time, whereas the typical “permabulker” is busy evolving a spare tire.

source Bill_Willis@T-nation.com

References

    1. Rennie MJ. Anabolic resistance: the effects of aging, sexual dimorphism, and immobilization on human muscle protein turnover. Appl Physiol Nutr Metab 2009;34:377-81.
    2. Kraegen EW, Cooney GJ. Free fatty acids and skeletal muscle insulin resistance. Curr Opin Lipidol 2008;19:235-41.
    3. Silveira LR, Fiamoncini J, Hirabara SM, Procopio J, Cambiaghi TD, Pinheiro CH, et al. Updating the effects of fatty acids on skeletal muscle. J Cell Physiol 2008;217:1-12.
    4. Danielsson A, Fagerholm S, Ost A, Franck N, Kjolhede P, Nystrom FH, et al. Short-term overeating induces insulin resistance in fat cells in lean human subjects. Mol Med 2009;15:228-34.
    5. Tremblay F, Marette A. Amino acid and insulin signaling via the mTOR/p70 S6 kinase pathway. A negative feedback mechanism leading to insulin resistance in skeletal muscle cells. J Biol Chem 2001;276:38052-60.
    6. Aguirre V, Werner ED, Giraud J, Lee YH, Shoelson SE, White MF. Phosphorylation of Ser307 in insulin receptor substrate-1 blocks interactions with the insulin receptor and inhibits insulin action. J Biol Chem 2002;277:1531-7.
    7. Beeson M, Sajan MP, Dizon M, Grebenev D, Gomez-Daspet J, Miura A, et al. Activation of protein kinase C-zeta by insulin and phosphatidylinositol-3,4,5-(PO4)3 is defective in muscle in type 2 diabetes and impaired glucose tolerance: amelioration by rosiglitazone and exercise. Diabetes 2003;52:1926-34.
    8. Belfort R, Mandarino L, Kashyap S, Wirfel K, Pratipanawatr T, Berria R, et al. Dose-response effect of elevated plasma free fatty acid on insulin signaling. Diabetes 2005;54:1640-8.
    9. Pedrini MT, Kranebitter M, Niederwanger A, Kaser S, Engl J, Debbage P, et al. Human triglyceride-rich lipoproteins impair glucose metabolism and insulin signalling in L6 skeletal muscle cells independently of non-esterified fatty acid levels. Diabetologia 2005;48:756-66.
    1. Myers MG, Jr., Munzberg H, Leinninger GM, Leshan RL. The geometry of leptin action in the brain: more complicated than a simple ARC. Cell Metab 2009;9:117-23.
    1. Schwartz MW, Woods SC, Porte D, Jr., Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature 2000;404:661-71.
    1. Rosenbaum M, Leibel RL. The role of leptin in human physiology. N Engl J Med 1999;341:913-5.
    1. Ahima RS, Saper CB, Flier JS, Elmquist JK. Leptin regulation of neuroendocrine systems. Front Neuroendocrinol 2000;21:263-307.
    1. Gregor MF, Hotamisligil GS. Thematic review series: Adipocyte Biology. Adipocyte stress: the endoplasmic reticulum and metabolic disease. J Lipid Res 2007;48:1905-14.
    1. Rosen ED, Spiegelman BM. Adipocytes as regulators of energy balance and glucose homeostasis. Nature 2006;444:847-53.
    1. Corcoran MP, Lamon-Fava S, Fielding RA. Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. Am J Clin Nutr 2007;85:662-77.
    1. Moro C, Bajpeyi S, Smith SR. Determinants of intramyocellular triglyceride turnover: implications for insulin sensitivity. Am J Physiol Endocrinol Metab 2008;294:E203-E213.
  1. Sitnick M, Bodine SC, Rutledge JC. Chronic high fat feeding attenuates load-induced hypertrophy in mice. J Physiol 2009;587:5753-65.