Nutrition
Are you one of those rapeseed oil guys who wouldn't eat anything with a face? Or are you a fish-eating machine that would eat pretty much any animal that doesn't wear a flea collar?
Regardless of your stance on meat vs. plant-based diets, if your goal is to look good naked, you'll probably be taking some sort of essential fatty acid supplement.
Linseed oil and fish oil are the most commonly consumed forms of essential fatty acids and many will consider these two sources of essential fatty acids to be interchangeable, but these two oils are distinctly different in many ways.
While both oils are rich in omega-3 fatty acids, there are distinct differences beyond the fact that flaxseed oil is suitable for vegetarians, while fish oil is not. Let's start with some basics about essential fatty acids. The two primary essential fatty acids (EFAs) are omega-3 and omega-6 fatty acids. These fatty acids are considered essential because your body cannot produce them itself and therefore they must be obtained from food.
|
Natural polyunsaturated omega-3 fatty acids |
Polyunsaturated omega-6 fatty acids |
|
Alpha-linolenic acid (LNA) |
Linoleic acid (LA) |
|
Stearidonic acid (SA) |
Gamma-linoleic acid (GLA) |
|
Eicosapentaenoic acid (EPA) |
Arachidonic acid (AA) |
|
Docosahexaenoic acid (DHA) |
|
Table 1: Adapted from Fats that Heal, Fats that Kill by Udo Erasmus
According to research by Simopoulos, the typical Western diet contains about 20 times as many omega-6 as omega-3 fatty acids. When you compare this to the 2:1 ratio that scientists consider ideal, it quickly becomes clear how suboptimal our diet is in this regard.
There are three reasons for this unhealthy ratio of omega-6 to omega-3 fatty acids in our diet:
- A deficiency of omega-3 fatty acids
- Excessive consumption of omega-6 fatty acids
- An inability of the body to convert dietary omega-3 fatty acids into omega-3 fatty acids that can be utilized by the body
The third point is the crux of the matter: can linseed oil fulfill its role as an omega-3 supplier?
Linseed oil is not an optimal source of omega-3 fatty acids
Twelve years ago, I looked into the effects of fish oil when a trainer at my gym complained of excessively dry skin on his hands during the winter. His hands looked as if they were covered in small cuts, some of which were even bleeding. When I asked him if he was taking omega-3 fatty acids, he told me that he was taking three tablespoons of linseed oil a day.
Referring to what I had read at the time, I recommended that he replace the linseed oil with fish oil for breakfast, lunch and dinner. And the result? Within a few days his hands healed completely - no more cracks and no more bleeding.
Why couldn't linseed oil do its job?
Linseed oil is one of the richest sources of alpha-linolenic acid (ALA) and contains over 50% ALA, which is why it is often referred to as one of the best sources of omega-3 fatty acids. The problem, however, is that the omega-3 fatty acids contained in linseed oil cannot be sufficiently converted into the actually important "players" in the body. The omega-3 fatty acids contained in linseed oil are simple ALS, which is a precursor to the magical EPA and DHA omega-3 fatty acids. However, just because linseed oil increases ALA levels in the blood does not mean that your body will convert this ALA into EPA and DHA. To confirm this, a 12-week study showed that linseed oil was not efficiently converted to DHA. Another study lasting 4 weeks showed that the EPA concentrations that could be achieved with the help of linseed oil were only half as high as when fish oil was used.
The inadequate conversion of ALA to EPA and DHA is related to competitive enzyme inhibition. Based on the fatty acid flow chart below, there are a number of intermediate steps that must be completed before ALA can be converted to EPA and then to DHA.
A very important enzyme called delta-6-desaturase (D6D) is required for this conversion.
Alpha-linolenic acid (linseed)
↓
Δ-6 Desaturase
↓
Octadecatetraenoic acid
↓
Elongase enzyme
↓
Eicosatetraenoic acid
↓
Δ5 Desaturase
↓
Eicosapentaenoic acid (EPA)
↓
Elongase enzyme
↓
Docosapentaenoic acid
↓
Δ4 Desaturase
↓
Docosahexaenoic acid (DHA)
Scientific research suggests that the amount of D6D decreases as we age. While we can't do much about the numbers on our birth certificate, it should be noted that diabetes, trans fats, alcohol and radiation have also been identified as causes of declining D6D levels.
If you're a regular reader of this site, then you should know how important blood sugar control is, so diabetes probably shouldn't be a concern. And if looking good naked is somewhere on your agenda, your trans fat consumption is likely to be minimal and your alcohol consumption below Lindsay Lohan levels.
As for radiation, it's everywhere. However, there are ways to minimize it. There are also some key nutrients you can supplement to build your D6D capacity, which include zinc and magnesium. Most of us are deficient in these two super minerals, which are crucial for many aspects of overall health.
(A tip on magnesium: if you have chocolate cravings all the time, this is a sign that you could be suffering from a magnesium deficiency. So if you've just eaten your child's birthday cake, you might want to get yourself some ZMA® ).
A second chance for flaxseed?
While flaxseed oil is probably not an effective way to get the amounts of EPA and DHA your body so desperately needs, flaxseed does have some benefits. Flaxseed is available in three forms: whole flaxseed, ground flaxseed and flaxseed oil. I prefer my clients to take whole flaxseed or ground flaxseed as both are an excellent source of fiber. Fiber helps cleanse the intestines and supports blood sugar control, which can lead to lower body fat levels.
Whole flaxseeds also contain lignans, which have been shown to affect estrogen levels. Many of my clients have symptoms of high estrogen levels and when I run hormone tests on them, 90% of them have elevated estradiol levels.
There are two primary reasons for this. Number one is estrogen mimicking compounds that are found in our environment called xenoestrogens. We are increasingly bombarded with xenoestrogens in the form of contaminated water and food, chemicals such as pesticides and herbicides, and plastics containing bisphenol A. The ugly thing about these little monsters is that they alter the conversion of cholesterol into steroid hormones.
Reason number two is the high activity of the enzyme aromatase. Aromatase is an enzyme that converts androgens like testosterone and androstenedione into estrogen. Remember all the hype about prohormones in the late nineties? Everyone had visions of cracking Mark McGuire's locker and reaching Bic Mac's proportions. Unfortunately, this is a prime example of something that looked good on paper but didn't work in the human body.
The main problem with androstenedione was that it can be converted into both testosterone and estrogen. So while some guys got more muscular and stronger from this stuff, others grew breasts and started asking their training partners if their training pants made their butts look bigger.
To reduce the amount of xenoestrogens you are exposed to, the first thing you need to do is reduce the amount of xenoestrogens you are exposed to. Limit the use of plastic, store your food in glass containers instead of plastic or Tupperware and never heat food in plastic packaging in the microwave. By doing so, you are giving your body real xenoestrogen injections.
As for aromatase, this is where the lignans in whole flaxseeds come in. Flaxseeds are the richest source of the plant lignan secoisolariciresinol diglucoside (SDG0) - a type of phytoestrogen similar in structure to endogenous sex hormones.
After consumption, the intestinal flora metabolizes SDG to enterodiol (ED) and enterolactone (EL), which are also known as mammalian lignans. There are studies that show that ED and EL both inhibit the aromatase enzyme.
Although I do not recommend flaxseed oil as a source of omega-3 fatty acids, I would recommend consuming flaxseed in shredded form or even as whole flaxseeds to inhibit the effects of the aromatase enzyme.
Use both to your advantage
In our world of Frankenstein foods and toxic fats, it's a smart idea to make omega-3 fatty acids a top priority - but relying on flaxseed oil is not such a good idea. Whether your goal is to build muscle, lose fat or boost your performance, an animal source of essential fatty acids like fish oil is much more effective than flaxseed oil.
But don't throw the flaxseed out with the fatty acid bath water. Whole or crushed flaxseeds still have important health benefits to offer. Try using a high quality fish oil supplement to meet your EPA and DHA needs and use some high fiber whole flaxseed for its benefits in blood sugar control and aromatase inhibition. While this may not help you land a vegan girlfriend, with more muscle, less fat and better overall health, I'd be very surprised if you have a hard time finding a carnivore to keep you company.
References
- Adlercreutz H, Bannwart C, Wähälä K, Mäkelä T, Brunow G, Hase T, Arosemena PJ, Kellis JT, Vickery LE. Inhibition of human aromatase by mammalian lignans and isoflavonoid phytoestrogens. J Steroid Biochem Mol Biol, 44:147-153, 1993
- Barceló-Coblijn G, Murphy EJ, Othman R, Moghadasian MH, Kashour T, Friel JK. Flaxseed oil and fish-oil capsule consumption alters human red blood cell n-3 fatty acid composition: a multiple-doing trial comparing 2 sources of n-c fatty acids. Am J Clin Nutr. 2008 Sep;88(3):801-9.
- Basch R, Bent S, Collins J, Dacey C, Hammerness P, Harrison M, Smith M, Szapary P, Ulbricht C, Vora M, Weissner W. Natural Standard Resource Collaboration. Flax and flax seed oil (Linum Usitatissimum) a review by the Natural Standard Research Colloboration. J Soc Integr Oncol 2007 Summer 5; (3): 92-105.
- Borriello SP, Setchell, KDR, Axelson M, Lawson AM. Production and metabolism of lignans by the human faecal flora. J Appl Bacteriol, 58:37-43, 1985.
- Erasmus, Udo. Fats that Heal Fats that Kill. Alive Books. Barnaby BC Canada. 1997.
- Simopoulos, Artemis. The Omega Diet. Harper Collins. New York, NY. 1999.
- Frye C, Bo E, Calamandrei G, Calzà L, Dessì-Fulgheri F, Fernández M, Fusani L, Kah O, Kajta M, Le Page Y, Patisaul HB, Venerosi A, Wojtowicz AK, Panzica GC. Endocrine Disrupters: a Review of SOMe Sources, Effects, and Mechanisms of Actions on Behavior and Neuroendocrine Systems. J Neuroendocrinol. 2011 Sep 27. doi: 10.1111/j.1365-2826.2011.02229.x. (Epub ahead of print)
- Horrin DF. Loss of delta-6-desaturase activity as a key factor in aging. Med Hypotheses. 1981 Sep;7(9):1211-1220.
- Lord, RS & Bralley JA. Laboratory Evaluations for Integrative and Functional Medicine. Duluth, GA: Metametrix Institute.
- Liu S, Baracos VE, Quinney HA, Clandin MT. Dietary omega-3 and polyunsaturated fatty acids modify fatty acyl composition and insulin binding in skeletal-muscle sarcolemma. Biochem J. 1994 May 1;299 (Pt 3): 831-7.
- Mantzioris, E, James MJ, Gibson RA, Cleland LG. Dietary substitution with an α-linolenic acid-rich vegetable oil increases eicosapentaenoic acid concentrations in tissues. Am J Clin Nutr-1994-Mantzioris-1304-9.
- Shimp JL, Bruckner L, Kinsella JE. The effects of dietary trilinoelaidin on fatty acid and acyl desaturases in rat liver. J Nutr. 1982 Apr;112(4):722-35.
By Robert Yang
How to end a diet without getting fat afterwards
You've found your abs - now what?
Dieting is a challenge, but the next phase is even harder. If you're not careful, things can get pretty ugly pretty quickly. Some refer to it as "reverse dieting". It's the phase after the diet and after the calorie restriction has ended. Reverse in this context means that you gradually start to increase your calorie intake again. It sounds simple, but your body is working against you.
The metabolic problem
After a fat loss diet, the goal is to find a new maintenance calorie intake. This calorie intake is the amount of calories you need to maintain your new body weight. How do you find this calorie amount? By slowly increasing your calories compared to your calorie intake during the diet. But there's a big problem.
Scientific research shows that your metabolic rate slows down after prolonged calorie restriction. Because of this reduced metabolic rate, your body prefers a fat-storing state on a physiological level. Not good. If you suddenly return your body to the amount of calories you were eating before you started your diet, you will build up body fat.
It's easy to decide on specific amounts of calories and macronutrients you want to target, but hunger can easily take on a life of its own and derail your good intentions. One spoonful of ice cream can easily turn into a whole carton. If this scenario becomes a habit, you'll experience rapid fat gain accompanied by a softer appearance, digestive issues, lack of energy and decreased motivation.
The hunger games
Prolonged calorie restriction will lead to increased hunger, a reduced metabolic rate and a decrease in activity.
Much of this is related to hormonal responses such as increases in ghrelin levels - also known as the hunger hormone - and decreases in levels of metabolic hormones such as T3 and T4. Scientists have observed this in men and women of all ages and body types, as well as in bodybuilders during competition preparation.
Dr. David Ludwig says, "Something has caused our fat cells to go into a calorie-storing turbo mode, causing them to soak up too many calories. As a result, there are too few calories in the bloodstream. So the brain does what it's supposed to do - it makes you hungry."
Many people claim to be hungrier after a diet than during the diet itself. When you lose weight, your hunger increases, while your energy expenditure decreases due to a reduction in non-exercise-induced thermogenesis (NEAT, a measure of calories burned through unconscious movement).
The opposite is true if your weight is above your set point and you consume more calories than you burn over a longer period of time: your appetite decreases and your thermogenic activity increases.
What can we do about this?
First of all, you should eat foods that help you minimize your hunger. After dieting, people overlook the food sources they choose and the cascade of hormonal responses these foods cause. The glycemic load of a meal has an impact on hunger (Note: glycemic load describes the quantity and quality of carbohydrates in a food or meal. A piece of watermelon and a donut have the same glycemic index but a very different glycemic load).
Think about the following. When dieting, people choose higher quality, minimally processed foods that are high in fiber and high in volume. They tend to choose carbohydrates with a lower glycemic index (e.g. sweet potatoes, green vegetables, whole grain oatmeal) and try to get full on fewer calories and by eating foods with a higher micronutrient content.
However, after eating this way during the diet, the dieter seems to forget what helped them achieve this body in the first place and may even feel entitled to eat the foods they gave up during their diet.
Even if the dieter has intentionally increased their fat and carbohydrate macronutrients to end the strict diet, this attempt to "normalize" their nutritional situation may cause them to feel more hungry than before. This is part of the reason that eating highly processed foods, which cause a rapid rise in insulin levels, will lead to increased fat storage and more post-meal hunger.
To understand this, we need to take a closer look at our hormones. A crucial aspect of your body's response to a meal is what happens to the hormones insulin and glucagon. Insulin is considered anabolic. It transports nutrients to your liver, your muscles and, unfortunately, your fat cells. Glucagon is considered catabolic. It helps the body break down stored nutrients such as glycogen and fat.
A study conducted by Dr. Ludwig looked at the effects of the glycemic index and hunger responses. The three subgroups of subjects were given different meals, all with the same calorie content, but one group ate a meal with a low glycemic load, one group ate a meal with a medium glycemic load and the third group ate a meal with a high glycemic load.
|
Meal with low glycemic load |
Meal with medium glycemic load |
Meal with a high glycemic load |
|
55g whole egg |
63.9g Wholemeal oat flakes |
60.9g Instant rolled oats |
|
45g egg white |
180g milk (2% fat) |
180g milk (2% fat) |
|
40g low-fat cheese |
15g cream |
15g cream |
|
200g spinach |
16g fructose |
19g dextrose |
|
30g tomato |
0g saccharin |
0,2g saccharin |
|
185g grapefruit |
397g water |
397g water |
|
115g apple slices |
|
|
|
Macronutrients (% carbohydrates/protein/fat) |
||
|
40/30/30 |
64/16/20 |
64/16/20 |
|
Energy density (KJ/g) |
||
|
2,46 |
2,52 |
2,52 |
The high GI group experienced the greatest increase in insulin levels, followed by a collapse. This group also had the weakest glucagon response. This is a recipe for fat storage.
Another interesting finding was the significant increase in adrenaline levels at the high GI meal compared to the low and medium GI meals. This insulin response strongly contributes to an increase in hunger as it mimics a response to a situation of (starvation).
The coolest thing about this study is that it tells us why people exceed their calorie and nutrient goals despite good intentions to stick with a specific plan. Members of the group that consumed the meal with the highest glycemic index consumed many more calories (600 to 700 kcal more) during the 5 hours following the meal than members of the other two groups. Maintaining good eating habits at one meal can therefore dramatically increase the likelihood that you will stay on plan for the next meal.
Another study showed very similar results. This study was a double-blind, cross-over design in which all groups consumed the same amounts of macronutrients. The meals differed only in the GI of the carbohydrates consumed. The group that consumed carbohydrates with a higher GI reported more hunger than the group that consumed carbohydrates with a low GI.
The most surprising result was that the activity of the nucleus accumbens was significantly increased in the group that consumed the high GI carbohydrates. This part of the brain is associated with dependence and addiction. In this area, your brain releases dopamine, which is why this area is also known as the feel-good center of the brain. This data gives us a clue as to why many people feel that they can no longer resist the urge to eat.
So when you're told that all carbs are the same and it doesn't matter if you eat your carbs in the form of sweet potatoes or donuts, it's important to remember that your body will react differently to those carbs regardless of the calories.
How you can combat the build-up of fat
Eat meals with a low glycemic load. Choose high fiber vegetables, low glycemic index carbohydrates and stick to a balanced diet. This will optimize the hormonal cascade after a meal and reduce your cravings so you stay full longer. Working with your body instead of against it will help you stay on track.
If you absolutely want to include highly processed foods in your daily diet, eat them before your workout. This may not be optimal for performance, but it will allow your body to use that glucose during exercise and reduce the likelihood of that glucose being stored as fat. This will prevent the negative reactions that would otherwise be seen.
Another tip: Various supplements such as chromium picolinate, cinnamon extract and even turmeric have been shown to help normalize blood sugar levels. This can improve the way additional carbohydrates are processed and used in your diet, while minimizing the risk of fat storage.
How should you increase your calories?
You need to get out of the calorie deficit and try to figure out what your new maintenance calorie amount is. The best approach to this will vary depending on how lean you want to stay and how your body responds to an increase in calorie intake. For some it will be perfectly fine to increase daily calorie intake by 500 kcal, while others will need to take a more conservative approach.
What makes this phase complicated is the fact that you can gain several kilos on the scales without putting on any fat. This is often simply the result of a replenishment of glycogen stores and a rebuilding of intramuscular triglycerides. You should be aware of this fact.
You should also remember that while it is important to pay attention to macronutrients, it is at least as important to make smart food choices that minimize your hunger so that you stay on track.
What about cardio training?
The best way to do cardio will vary from person to person based on numerous different factors: how much cardio you've done before, what type of cardio, what intensity, etc. Using high-intensity interval training (HIIT) as your primary form of cardio is an excellent choice, according to one idea.
HIIT will significantly increase your EPOC (post-exercise oxygen consumption) - also known as the afterburn effect - which means it will rev up your metabolism, which has been impaired in its rate. You will burn more calories during the rest of the day and be better able to cope with the extra calories you consume after the diet.
HIIT will also affect your strength adaptations to your weight training much less, if at all, compared to low intensity cardio. If you have experienced a loss of strength during your diet, the last thing you want to do is exacerbate this strength deficit with too much incorrect cardio training.
HIIT can also help you maintain your muscle mass and has even been shown in some studies to induce a hypertrophy response, while cardio training at a consistent lower intensity can attenuate the protein synthesis (muscle growth) response to weight training.
As your metabolism recovers over time, you should reduce the number of cardio training sessions and their duration.
References
- Pardue A. Case Study: Contest Preparation Diet Effects On A Drug-Free Bodybuilder. May 2016.
- Rossow LM, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural bodybuilding competition preparation and recovery: A 12-month case study. International Journal of Sports Physiology and Performance. 2013;8(5):582–592. doi:10.1123/ijspp.8.5.582.
- Kistler BM, Fitschen PJ, Ranadive SM, Fernhall B, Wilund KR. Case study: Natural bodybuilding contest preparation. International Journal of Sport Nutrition and Exercise Metabolism. 2014;24(6):694–700. doi:10.1123/ijsnem.2014-0016.
- De Pergola, G., et al. "Free triiodothyronine and thyroid stimulating hormone are directly associated with waist circumference, independently of insulin resistance, metabolic parameters and blood pressure in overweight and obese women." Clinical endocrinology 67.2 (2007): 265-269.
- Reinehr, T., and W. Andler. "Thyroid hormones before and after weight loss in obesity." Archives of disease in childhood 87.4 (2002): 320-323.
- Greenway FL. Physiological adaptations to weight loss and factors favoring weight regain. International Journal of Obesity (2005).
- Ludwig, David S., et al. "High glycemic index foods, overeating, and obesity." Pediatrics 103.3 (1999): e26-e26.
- Lennerz, Belinda S., et al. "Effects of dietary glycemic index on brain regions related to reward and craving in men." The American journal of clinical nutrition 98.3 (2013): 641-647.
- Docherty JP, Sack DA, Roffman M, Finch M, Komorowski JR. A double-blind, placebo-controlled, exploratory trial of chromium picolinate in atypical depression: effect on carbohydrate craving. J Psychiatr Pract. 2005 Sep;11(5):302-14.4.
- Safdar, Mahpara, et al. "Effect of various doses of cinnamon on blood glucose in diabetic individuals." Pakistan Journal of Nutrition 3.5 (2004): 268-272.
- Helms, E. R., et al. "Recommendations for natural bodybuilding contest preparation: resistance and cardiovascular training." Journal of Sports Medicine Physical Fitness 55 (2015): 164-178.
- Borsheim E, Bahr R. Effect of exercise intensity, duration and mode on post-exercise oxygen consumption. Sports Med. 2003;33(14):1037-1060
- Wilson JM, Marin PJ, Rhea MR, Wilson SM, Leoneeke JP, Anderson JC. Concurrent training: a meta analysis examining interference of aerobic and resistance exercise. J. Strnegth Cond. Res. Oct 13 2011.
By Christopher Barakat
Source: https://www.t-nation.com/diet-fat-loss/ditch-your-diet-stay-ripped
Control them and get hard and defined more easily
When you think of hormones, especially in the fitness and bodybuilding world, you probably think of things like testosterone, insulin, cortisol and growth hormone. You probably won't think of GLP and GIP.
GLP and GIP are hormones of the digestive tract and your ability to get hard and defined can stand or fall with them. The funny thing is, most people have never heard of these hormones and even experts didn't fully understand their full impact until recently.
The unexpected revelations of a gastric bypass
Gastric bypass surgery has become the treatment of choice for severely obese patients. This surgery can also be seen as proof that the calorie model of metabolism is correct.
When this surgery was originally developed, the idea was to reduce the volume of food that could be eaten. It was believed that the observed fat loss was based solely on the fact that patients were eating less or absorbing less food. It was believed that this reduced calorie intake was the only reason for the weight loss.
If you physically reduce the size of the stomach, then the patient can't eat as much as before and loses weight. That was the theory and reducing calorie intake definitely plays a role. But is that the whole story?
Slowly, a new understanding of what is happening developed. There is an unintended and only recently discovered consequence of these gastric bypass operations: reduced hunger and (to a lesser extent) reduced cravings. How can this be? This surgery does not take place in the brain, which is the area that controls these feelings.
Even more interesting is the fact that in a high percentage of patients who suffered from diabetes or insulin resistance before the surgery, these problems disappeared completely. Imagine that before the surgery you were plagued by constant hunger, insatiable cravings and diabetes and as you recover from the surgery you realize that your hunger and cravings have disappeared and your diabetes has been cured.
What is happening here?
The positive effects that this surgery has on metabolism and weight loss are not simply a matter of calories, but are related to an unintended manipulation of the endocrine properties of the mucous membranes of the digestive tract. Endocrine in this context refers to the hormonal activity of the digestive tract.
The digestive system is not simply a place where food is digested and absorbed. The digestive system also secretes hormones.
In order to absorb food and regulate metabolism, the body needs a way to enable communication between the brain, pancreas and other organs and tissue types regarding the type of food being fed. Is the food a large bowl of sweet cereal that requires a large amount of insulin? Or is it a huge steak that will linger in the stomach for a while to be digested?
Our digestive tract is lined with sensory cells that "examine" the food that has been eaten. These cells provide the body with information about the quantity and composition of the food consumed and send signals via hormones/peptides to the brain, pancreas, fat cells, etc.
It is now believed that these hormones of the digestive tract are the primary mechanism by which these operations exert their effects.
GLP and GIP
The glucose-dependent insulinotropic peptide (GIP) and the glucagon-like peptide (GLP) are probably the two most important hormones. These hormones are also known as incretins.
These two hormones switch off hunger in the brain and stimulate the release of insulin as soon as they perceive large amounts of glucose. These two hormones are the reason why glucose injected directly into a vein causes much less insulin to be released than the same amount of glucose consumed.
GIP is secreted by so-called K sensory cells that line the digestive tract in the upper small intestine where food leaves the stomach (the duodenum). GLP is secreted by the L sensory cells, which are also located in the duodenum, but have a higher concentration in the lower part of the intestine.
With gastric bypass, GIP concentrations are reduced while GLP levels are increased. This is because the area of the intestine that contains most of the GIP-secreting cells is bypassed and no longer has contact with the food, while most of the areas that secrete GLP remain intact.
GIP and GLP have very different effects on metabolism, they both suppress appetite and both cause insulin secretion (but only in the presence of glucose). Obese people and diabetics have reduced GLP activity and the influence of GIP on the pancreas is suppressed.
GPL has several effects that make it very beneficial for diabetics and obese people compared to GIP. GLP reduces the levels of the hormone glucagon - a hormone that is out of control in diabetes and causes glucose to be continuously released from the liver. GLP also helps the body to produce new, more functional pancreatic cells, restoring the correct function of the insulin mechanism.
GLP also reduces the breakdown of muscle tissue. It also slows down the release of food from the stomach, which means that other hunger hormones (such as ghrelin) remain suppressed for longer.
All of this leads to more GLP, less GIP, lower glucagon levels (which normalizes blood sugar), restoration of insulin sensitivity and reactivity, suppressed appetite, reduced cravings and increased fat burning. These changes positively influence the amount of calories consumed.
Note: We do not yet know how long this effect lasts, as some patients regain the weight they have lost over the years, but rarely to the weight they once had.
What does this mean for us?
All of this shows us that weight loss is not simply a matter of calorie math, but involves complex interactions of hormonal biochemistry.
Most people do not need to undergo expensive and risky surgery to reap the same effects and benefits. GLP and GIP levels can also be manipulated with food. Fiber (especially viscous fiber), protein, bitter foods, probiotics and other factors are also able to manipulate the sensory cells of the digestive tract, thereby reducing hunger, helping with cravings and restoring insulin sensitivity.
How can you use this science for fat loss?
- Use GIP and GLP to your advantage by eating foods that stimulate their appetite suppressing effects but not their insulin stimulating effects. This means protein, fat and fiber without starch and sugar. Protein, fat and fiber will all have an impact on GIP and GLP, and as long as you don't eat large amounts of starch or sugar during the same meal, you will get full faster and stay full longer.
- Never combine fat and starch/sugar. This combination will greatly increase GIP levels and lead to higher insulin secretion over time.
- Choose viscous fiber. This type of fiber lines the digestive tract and makes it "think" there is more food in the digestive tract than there really is. Using a fiber-based drink as a snack is an excellent way to take advantage of this effect. The best fibers for this purpose are oat bran, acacia and glucomannan. But be careful, because if these fibers are consumed in combination with sugar or starch, you can achieve exactly the opposite effect. Remember that you are using fiber to control your appetite, not to eliminate it. Avoid products that are designed to eliminate appetite and are overloaded with sweeteners.
- Eat the right carbohydrates. High-fiber carbohydrates such as non-starchy vegetables and less sweet fruits have the best fiber to sugar/starch ratio. These are the carbohydrates you should prioritize.
- Branched-chain amino acids - and leucine in particular - can have a special effect on GLP. A BCAA supplement that is used as a snack and not simply to promote post-workout recovery may be a wise choice.
References
- Shalev A1, Holst JJ, Keller U. Effects of glucagon-like peptide 1 (7-36 amide) on whole-body protein metabolism in healthy man. Eur J Clin Invest. 1997 Jan;27(1):10-6.
- Vendrell J1, et al. Study of the potential association of adipose tissue GLP-1 receptor with obesity and insulin resistance. Endocrinology. 2011 Nov;152(11):4072-9. doi: 10.1210/en.2011-1070. Epub 2011 Aug 23.
- Chen Q1, Reimer RA. Dairy protein and leucine alter GLP-1 release and mRNA of genes involved in intestinal lipid metabolism in vitro. Nutrition. 2009 Mar;25(3):340-9. doi: 10.1016/j.nut.2008.08.012. Epub 2008 Nov 26.
- Bueter M1, le Roux CW. Gastrointestinal hormones, energy balance and bariatric surgery. Int J Obes (Lond). 2011 Sep;35 Suppl 3:S35-9. doi: 10.1038/ijo.2011.146.
- Tadross JA1, le Roux CW. The mechanisms of weight loss after bariatric surgery. Int J Obes (Lond). 2009 Apr;33 Suppl 1:S28-32. doi: 10.1038/ijo.2009.14.
- Shin AC1, Berthoud HR. Food reward functions as affected by obesity and bariatric surgery. Int J Obes (Lond). 2011 Sep;35 Suppl 3:S40-4. doi: 10.1038/ijo.2011.147.
By Dr. Jade Teta
Source: https://www.t-nation.com/diet-fat-loss/the-hidden-fat-loss-hormones
Although branched-chain amino acids (BCAAs) have many interesting properties on their own and can help to promote and optimize anabolic and anti-catabolic processes, BCAAs and glutamine represent a powerful synergistic combination that is in many ways clearly superior to the use of BCAAs or glutamine alone.
While BCAAs are the most abundant amino acids in muscle protein, glutamine is the most abundant free amino acid in the bloodstream and cells. Glutamine is essential for the function of the immune system and the cells involved in the regeneration and repair of muscle tissue. In addition, glutamine is said to have many other beneficial effects, ranging from healing the stomach lining to being used as a supplement to reduce cravings for alcohol and nicotine.
Similar to BCAA levels, it has been shown that there is a correlation between the concentration of glutamine in the body and the rate of protein synthesis. In other words, glutamine levels are a good indicator of an anabolic state. When blood glutamine levels are high, the chances of positive adaptations in muscle mass and strength in response to weight training are higher and low blood glutamine levels are a clear sign of overtraining and/or malnutrition. The synergy between BCAAs and glutamine exists because not only do both induce many of the same anabolic and anti-catabolic effects, but BCAAs can directly contribute to increasing glutamine stores under stressful conditions by serving as precursors for the formation of glutamine.
A combination of glutamine and BCAAs has been shown to dramatically improve nitrogen balance and reduce muscle breakdown in patients with burns and after major surgery. In addition, a relatively low-dose combination of 3 grams of BCAAs and 5 grams of glutamine has been shown to produce significantly greater gains in muscle mass and strength in athletes than whey protein alone. Anecdotal reports suggest that some athletes can make significantly greater gains when using higher doses of BCAAs and glutamine in conjunction with optimal nutrition and training. Although BCAAs and glutamine have many benefits on their own, the combination of these two supplements appears to significantly increase the potential benefits.
What is the correct dosage?
In order to maximize the numerous anabolic effects of BCAAs and glutamine, it is important that sufficiently high dosages are used. Although it has been shown that as little as 3 grams of BCAAs per day can provide benefits, studies using higher doses of BCAAs in the range of 20 grams per 50 kilograms of lean body weight show much more dramatic results. Even better results can be achieved during intense training phases or a strict diet with BCAA dosages of up to 0.45 grams per kilogram of lean body mass. The optimum dosage for this purpose can be easily calculated by subtracting the weight of the body fat from the body weight and multiplying the result by 0.45. So if you weigh 100 kilos and have a body fat percentage of 10%, then your fat-free body mass is 90 kilos, which, multiplied by 0.45, results in a quantity of approx. 40 grams of BCAAs per day.
The minimum dosage for glutamine is 0.1 grams per kilogram of lean body mass. However, significantly better results are achieved with dosages of between 0.2 and 0.45 grams of glutamine per kilogram of lean body mass. The same trainee with a body weight of 100 kg and a body fat percentage of 10% should therefore consume between 10 and 40 grams of glutamine per day, whereby the higher dosages make the most sense, particularly during intensive training phases in conjunction with a high calorie deficit and a reduced carbohydrate intake.
The right timing
Perhaps the biggest differences of opinion among experts in the field of BCAA or glutamine supplementation are regarding the correct timing of these nutrients. Depending on who you ask, you will get different answers. I think everyone agrees that the greatest physical stress on an athlete occurs during training sessions or sporting events. Since BCAA and/or glutamine supplementation provides its greatest benefits during these periods of peak stress, it makes sense that supplementation with these compounds should take place prior to training to ensure that high levels of BCAAs and glutamine are present in the body during exercise.
It is important to remember that dietary protein is broken down in the digestive tract into individual amino acids including BCAAs and glutamine. It is also important to remember that carbohydrates will help to conserve BCAA and glutamine stores in the body. If you eat well, provide your body with adequate protein at regular intervals and maintain a normal lifestyle, then there should be sufficient amounts of BCAAs and glutamine in your body for most of the day. However, when a sudden catabolic load is placed on the body during exercise, BCAA and glutamine stores are drawn upon as glycogen stores begin to be depleted.
This is the time when strategically increased BCAA and glutamine levels will have their greatest anabolic and anti-catabolic effect. For this reason, the first thing to do is to ensure high BCAA and glutamine levels during training by splitting the daily dosage of these two nutrients in half, taking the first half 30 minutes before training or at the start of the training session and the second half immediately after training. This way you will get the most bang for your buck. You should try this approach for two weeks and see if you notice a substantial difference in terms of recovery, delayed onset muscle soreness, fat loss, muscle growth and energy levels during training.
There will of course be additional benefits if you increase your daily BCAA and glutamine dosage and use these supplements at other times of the day. During a strict diet, where both calorie intake and carbohydrate intake are significantly reduced, supplementing with 2 to 5 grams of BCAAs and glutamine between meals will help maintain a positive nitrogen balance and protect existing muscle mass from breakdown. In addition, glutamine between meals can help reduce cravings for sweets and carbohydrates. Another point that should not go unmentioned is the effect on the release of growth hormone.
Both BCAAs and glutamine have been shown to independently increase growth hormone levels when using a dosage of just 3 grams. By using 3 to 5 grams of BCAAs and 3 to 5 grams of glutamine between meals and an additional 5 to 10 grams of glutamine before bed, athletes - and especially athletes over the age of 30 - can benefit from increased growth hormone levels. This can lead to a lower body fat percentage, increased energy and accelerated regeneration after training.
"Why does my breakfast make me hungry?" After someone asked me this question for who-knows-how-many times, I decided to delve deeper into the possible reasons and mechanisms. I thought it would be a good idea to share my thoughts on the subject with you.
The average person eats their breakfast
So what happens when you start eating? Bad things? No, not necessarily, depending on the other variables in this equation - more on that very soon.
Welcome to the average guy, who is about as average as it gets - with all the implications that means he's fat, has poor insulin sensitivity and is out of shape - so he fits the standard of modern man used in the scientific literature.
The average guy sits down and eats his breakfast and, due to the influence of cortisol, his pancreas responds with a rapid and - relative to other times of the day when all else is equal - strong insulin release. This lowers blood glucose levels back to baseline more quickly than later in the day, which is a desirable effect in this context.
Although the food-induced insulin peak occurs much faster and is much higher due to the coincidence with the peak cortisol daily rhythm, the net effect should be that average insulin secretion and average blood glucose levels are lower during the breakfast phases than later in the day when food intake occurs at low cortisol levels. In some ways, our average guy's sluggish pancreas might even benefit from the increased insulin response in the morning.
That was our average guy. But what about an above average fit person? This is where things start to get interesting.
Insulin sensitivity and insulin resistance: a brief introduction
I've noticed something very strange and I've observed it far too often to dismiss it as coincidental.
When I first started dieting, I was doing well with a typical high meal frequency with the typical fitness-oriented, oatmeal-based breakfast. I started out quite fat at around 100 kilos and lost almost 20 kilos using a fairly generic approach.
Of course, I made rookie mistakes galore - especially in the cardio area where I overdid it - and suffered as a result. I had my setbacks - like everyone else - but I got through them all.
However, it took a while in terms of my leanness before breakfast started to become a problem. First of all, I always felt that it was an unnecessary caloric burden that interfered with my dieting. I wasn't hungry in the morning, but I was even hungrier in the evening.
Of course, if I had known better back then, I would have started skipping breakfast sooner, but back then everyone was preaching the important benefits of breakfast and I didn't really dare to break all those golden rules of fitness.
Secondly, it seemed like the post-breakfast hunger pangs would increase in both frequency and strength with every damn gram of body fat I lost after a certain point. At a certain point, this hunger became excessive and that's when I started to tread water in terms of progress. This continued until I decided to do my own research and stop swallowing the nonsense that so-called fitness gurus and other dubious sources were feeding me. The rest is history.
Anyway, let me put on my lab coat and explain to you how this fits in with everything I've told you so far. We have now reached the second key point in this hypothesis behind the phenomenon of hunger after breakfast. The first key point, as you may remember, was the Cortisol Awakening Response (CAR) and its maximum value, which coincides with breakfast.
The second key point is insulin sensitivity. What happens when a person with high insulin sensitivity eats something? In a nutshell, rising blood glucose levels send a signal to the pancreas and the pancreas responds with insulin. The insulin then transports the glucose from the blood to places where it is needed (e.g. liver and muscles), lowering blood glucose levels and preventing glucose from accumulating in the blood.
When blood glucose levels are elevated for an extended period of time (as seen in untreated type 2 diabetes, insulin resistance, poor insulin sensitivity, etc.) this causes all kinds of bad things to happen, which is the reason we should try to bring them back down to baseline as quickly as possible. This is the reason that high insulin sensitivity is a good thing.
When your body has a high insulin sensitivity, your pancreas responds quickly to glucose with a strong insulin surge, which slowly subsides when it is no longer needed. A rapid rise in insulin levels followed by a rapid drop. The net result is lower blood glucose and insulin levels after eating.
In contrast, insulin resistance results in a sluggish insulin response with a small insulin surge followed by a slow drop in insulin levels. The net result is higher blood sugar and insulin levels after eating.
Imagine a graph showing insulin release in the post-meal phase with time on the x-axis and insulin levels on the y-axis. Now imagine a pulse-like pattern for a person with high insulin sensitivity and a mountainous pattern for an insulin-resistant person - this is what it would look like.
An important point in the above scenario is that insulin levels reach a higher maximum in the person with high insulin sensitivity.
Insulin and blood glucose regulation
Remember that cortisol increases insulin secretion. If you have high cortisol levels (e.g. at peak CAR) and eat something, insulin secretion will be boosted. Your pancreas reacts faster and more strongly.
But our fit example person already has a really robust insulin response because they have a high insulin sensitivity. And now add to that the enhancing effect of CAR on insulin secretion. What do you get? In theory, a very strong and sharp insulin pulse. And what is the consequence of this?
In other words - just as an example - what is the consequence of injecting too much insulin relative to your needs? If you overdo it with this, you risk all the serious consequences of life-threatening hypoglycemia, resulting in extreme hunger, confusion, coma, brain damage and death - in that order.
While the above is a real danger for diabetics, there is no such danger for healthy individuals. Over the course of evolution, we have developed an extremely efficient regulatory system to prevent our blood sugar levels from dropping too low, to the point where our bodily functions and cognition are impaired and our chances of survival are reduced.
In fact, blood glucose regulation is a very safe system with redundant mechanisms that are able to increase glucose release to meet our needs even if one system fails. Glucagon, epinephrine (adrenaline), cortisol and growth hormone are different hormones that work together to fulfill each other's role in the event that one cannot do its job properly.
But this system has not evolved to take care of blood sugar levels that are just low enough to trigger hunger without having serious side effects beyond that. In fact, low blood sugar levels as a hunger signal were the focus of one of the earliest theories of appetite regulation.
Why does breakfast make the average fit person hungry?
As part of the "glucostatic theory", Jean Mayer postulated in the 1950s that blood sugar served as the primary hunger-inducing signal that made us want to eat (Mayer, 1953). Later studies have taught us that appetite regulation is far more complicated, but that blood sugar plays a clear role in the equation.
Building on Mayer's theory, Campfield proposed a more complex and refined theory in which, in brief, he suggested that falling blood glucose levels could serve as a hunger signal (Campfield & Smith, 2003). This has been echoed elsewhere in the sense that the rate at which blood glucose levels fall may in some sense serve as an alarm signal - while a prompt drop in blood glucose levels after eating is desirable, too sharp and rapid a drop may be interpreted as a danger and trigger a hunger signal.
So if our insulin-sensitive, fit person eats their breakfast directly to the maximum value of the Cortisol Awakening Response (CAR), then a lot of insulin is released in response to this meal, resulting in a rapid drop in blood glucose levels.
Now let's look at the meal itself. What does the typical breakfast of a fit person look like? Chances are that this meal is high in protein and carbohydrates, low in fat and quite often includes a source of dairy or milk protein. Each of these components independently contributes further to insulin secretion.
As a consequence of the above, hunger rears its ugly head shortly after a meal. Either as a result of blood sugar levels dropping a little too low or as a result of it dropping too quickly within a narrow window of time.
Let's put it all together
And that, my friends, was my abbreviated version of the explanation for post-breakfast hunger. When I think about it a bit, it fits perfectly with my personal experience, my observations and many anecdotes I've heard over the years.
Hunger after breakfast is something that occurs more frequently and to a greater extent in fairly lean people. I would estimate that this phenomenon is quite common in the 12 to 14% body fat range. And as you approach a single-digit body fat percentage, this phenomenon is indeed quite common - and becomes a serious obstacle for many.
As we get leaner, our insulin sensitivity gradually improves. And as insulin sensitivity increases step by step, we get hungry faster after breakfast and this hunger becomes more and more annoying until we finally wonder why we feel like we are starving 1 to 2 hours after a reasonable sized meal.
In a sense, it's funny that blood sugar regulation works best in the fasting state and not in the aforementioned breakfast scenario. This becomes understandable when you consider that in the fasting state there is a balance between supply and removal - in this case glucose and insulin. Blood glucose levels are low and are well maintained by low insulin levels in a person with good insulin sensitivity.
After breakfast, clearance is disproportionate to intake (breakfast) due to cortisol - an imbalance that would not occur in other circumstances (i.e. the same meal later in the day with low cortisol or in a person with lower insulin sensitivity).
All this raises interesting questions about the role of the cortisol-insulin link - or breakfast consumption and adaptation (or lack of adaptation) in the course of human evolution and its consequences for modern humans with their modern meal pattern.
This is very interesting indeed when you consider the events that take place at a metabolic and transcriptional level when you combine cortisol and insulin. Not to mention the role of cortisol in conditioning and getting leaner and the fact that even if breakfast first thing in the morning is an artificial habit coined by one of the first and possibly biggest giants of the food industry (Kellogs), this habit is certainly one that we get into very quickly.
But that's a topic for another time. Or for another person intelligent enough to recognize the references to something I've just made - always assuming anyone cares at all.
Final reflection
In conclusion, I would like to emphasize that there are a few things I had to leave out, as this article has already become quite long. I should perhaps at least mention these briefly and succinctly by saying that there is a high degree of individual variance in the Cortisol Awakening Response and that this could also influence insulin secretion (i.e. a stronger Cortisol Awakening Response could have a greater influence on food-induced insulin secretion).
In addition, food and macronutrient choices obviously play a large role in all of this, but this role may be different than most would expect. For example, some protein sources - or should I say amino acids - are not only highly insulinogenic, but also elicit a cortisol response. Coincidentally, these tend to be the protein sources that are often consumed at breakfast.
Perhaps I should mention that protein can elicit a cortisol response depending on the context (Benedict et al., 2005; Gibson et al., 1999; Slag et al., 1981). Oh, you thought it was the other way around - that protein lowers cortisol levels? Well, then you've learned something new today.
References
- Benedict, C., Hallschmid, M., Scheibner, J., Niemeyer, D., Schultes, B., Merl, V., Fehm, H. L., et al. (2005). Gut protein uptake and mechanisms of meal-induced cortisol release. The Journal of clinical endocrinology and metabolism, 90(3), 1692-1696. doi:10.1210/jc.2004-1792
- Campfield, L. A., & Smith, F. J. (2003). Blood glucose dynamics and control of meal initiation: a pattern detection and recognition theory. Physiological Reviews, 83(1), 25-58. doi:10.1152/physrev.00019.2002
- Clow, A., et al, The cortisol awakening response: More than a measure of HPA axis function. Neurosci. Biobehav. Rev. (2010), doi:10.1016/j.neubiorev.2009.12.011
- Dallman MF, Akana SF, Strack AM, Hanson ES, Sebastian RJ. The neural network that regulates energy balance is responsive to gluco- corticoids and insulin and also regulates HPA axis responsivity at a site proximal to CRF neurons. Stress: Basic Mechanisms Clin Implicat 1995; 771: 730±742.
- Fries, E., Dettenborn, L., Kirschbaum, C., 2009. The cortisol awakening response (CAR): facts and future directions. Int. J. Psychophysiol. 72, 67-73.
- Gibson, E. L., Checkley, S., Papadopoulos, A., Poon, L., Daley, S., & Wardle, J. (1999). Increased salivary cortisol reliably induced by a protein-rich midday meal. Psychosomatic Medicine, 61(2), 214-224.
- MAYER, J. (1953). Glucostatic mechanism of regulation of food intake. The New England journal of medicine, 249(1), 13-16. doi:10.1056/NEJM195307022490104
- Newport, D.J. and Nemeroff, C.B. (2002) Stress. In: (Ed. in chief), Encyclopedia of the Human Brain, Vol. 4. Elsevier, pp. 449-462.
- Shin, I.-Y., Ahn, R.-S., Chun, S.-I., Lee, Y.-J., Kim, M.-S., Lee, C.-K., & Sung, S. (2011). Cortisol Awakening Response and Nighttime Salivary Cortisol Levels in Healthy Working Korean Subjects. Yonsei Medical Journal, 52(3), 435. doi:10.3349/ymj.2011.52.3.435
- Slag, M. F., Ahmad, M., Gannon, M. C., & Nuttall, F. Q. (1981). Meal stimulation of cortisol secretion: a protein induced effect. Metabolism, 30(11), 1104-1108.
- Therrien, F., Drapeau, V., Lupien, S. J., Beaulieu, S., Doré, J., Tremblay, A., & Richard, D. (2008). Awakening cortisol response in relation to psychosocial profiles and eating behaviors. Physiology & Behavior, 93(1-2), 282-288. doi:10.1016/j.physbeh.2007.08.019
- Vila, G., Krebs, M., Riedl, M., Baumgartner-Parzer, S. M., Clodi, M., Maier, C., Pacini, G., et al. (2010). Acute effects of hydrocortisone on the metabolic response to a glucose load: increase in the first-phase insulin secretion. European journal of endocrinology / European Federation of Endocrine Societies, 163(2), 225-231. doi:10.1530/EJE-10-0282
