1.1g for women and 1.6g for men
Epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), glucagon, growth hormone, and thyroxine (T4)
Saturated (SFA), Monounsaturated (MUFA), and Polyunsaturated (PUFA)
To transport cholesterol to tissues where it may be used for membrane construction or conversion into other metabolites
At least 20% of total energy intake
95%
<ol class="tight" data-tight="true"><li><p>Fatty acids</p></li><li><p>Triacylglycerols</p></li><li><p>Diacylglycerols</p></li><li><p>Monoacylglycerolds</p></li><li><p>Waxes (esters of fatty acids)</p></li></ol><p></p>
Linoleic acid (LA) and α-linolenic acid (ALA)
<p>To reverse cholesterol transport by collecting cholesterol from tissues and blood and transporting it to the liver for excretion. HDL is basically the cholesterol clean up crew.</p>
At least 7.2 mg dietary cholesterol per kg of lean body mass or more than 400 mg in men
Trans fatty acids
Over 2g combined EPA + DHA per day
EPA, DHA, and ALA
Diabetes, brain and heart toxicity, infertility, coronary heart disease, depression, and Alzheimer’s disease
12g for women and 17g for men
Lipolysis
Closer to 1:1 but no more than 4:1
<ol class="tight" data-tight="true"><li><p>Cause inflammation</p></li><li><p>Increase LDL cholesterol levels</p></li><li><p>Decrease HDL cholesterol levels</p></li><li><p>Distort cell membranes</p></li></ol><p></p>
<p>PUFAs have multiple double carbon bonds which are at risk of converting to trans fat when processed at high temperatures for a substantial amount of time. SFAs do not have any double carbon bonds so they are not at risk of being converted to trans fat. MUFAs only have a single double carbon bond so the risk of converting to trans fat is very minimal.</p>
<p>10-15% of total daily kcal<br>Absolute minimum of 20 g for women and 30 g for men<br>Over 20% or 44-56 g is generally advisable</p>
<ol class="tight" data-tight="true"><li><p>Phospholipids</p></li><li><p>Glycolipids</p></li><li><p>Lipoproteins</p></li></ol><p></p>
<p>An increased fat intake can improve the endogenous production of anabolic hormones and also possibly by alter muscle cell membrane functioning.</p>
<p>Women’s metabolisms are more protein- and glucose-sparing than men’s in comparison and so they preferentially oxidize fat for fuel/energy (fat is the generally preferred energy substrate). Dietary fat can also be more satiating in women than men. An increase in dietary fat can also help in greater estrogen production which is beneficial for women.</p>
<p>It is not how much testosterone per se that someone has but rather the amount of androgen receptors which predicts how much muscle mass someone can gain. An individual can have as much testosterone as someone else, but if the other person has more androgen receptors, then that individual likely has a greater propensity for building for muscle. The other person may also have a stronger affinity for the receptor, a higher amount of unbound testosterone, or less antagonistic activity on the androgen receptor.</p>
<p>AAS users do not benefit from anabolic hormonal benefits that increased fat intake provides to natural trainees as they are already providing themselves with amounts of exogenous testosterone that are above and beyond what the body can produce naturally.</p>
<p>metabolized<br>digested<br>absorbed</p>
<p>exogenous; endogenous</p>
<p>Chylomicrons are lipoproteins that transport dietary fat metabolites after their digestion and absorption. They are effectively taxi drivers for fats.</p>
<p>No. The small intestine can digest up to 600 g of triacylglycerols with 95% efficiency.</p>
<p>Short- and medium-chain fatty acids are transported directly to the liver from the small intestine.<br><br>Long-chain fatty acids must first be packaged into chylomicrons before being transported to the tissues that need them (e.g., muscle and adipose tissue).</p>
<p>lipoprotein lipases<br>chylomicrons<br>VLDLs<br>TAGs<br>cholesterol</p>
<p>BF% is generally determined by how full a person’s adipocytes are, not the number of adipocytes. After adolescence, the number of adipocytes a person has stays relatively constant and would only materially increase if the person experienced significant fat gain (adipogenesis).</p>
<ol class="tight" data-tight="true"><li><p>Glucose is metabolized to make acetyl-CoA which can be converted to fatty acids.</p></li><li><p>Lipoprotein lipase acts on triacylglycerols (TAG) in chylomicrons and free fatty acids (FFA), diacylglycerols (DAG), and glycerol enter the adipocyte. Glycerol cannot be used and is excreted back into the bloodstream.</p></li><li><p>Lipoprotein lipase acts on VLDLs so TAG, FFA, DAG, monoacylglycerols (MAG), and cholesterol enter the cell.</p></li><li><p>The pathways favor energy storage as TAG. Insulin stimulates lipogenesis by promoting entry of glucose into the adipocyte (cell) and inhibiting the lipoprotein lipase from hydrolyzing the stored TAG into FFA and glycerol.</p></li></ol><p></p>
<ol class="tight" data-tight="true"><li><p>When fatty acids and glycerol are not immediately used for energy or fat storage, they are transported to the liver to be converted into nutrients that are more useful to the body. The liver is the body’s main nutrient repackaging site.</p></li><li><p>In the liver, glycerol can serve as a substrate for glucose via gluconeogenesis or new triglycerides by combining with three fatty acids. </p></li><li><p>The liver can also create its own glycerol and fatty acids.</p></li><li><p>The liver can also convert fatty acids into ketones.</p></li></ol><p></p>
<p>blood glucose levels</p>
<p>Hyperglycemia (high blood sugar levels) triggers the release of insulin which promotes glucose uptake into adipocytes causing lipogenesis to occur instead of lipolysis.<br><br>Hypoglycemia (low blood sugar levels) results in a reduced supply of intracellular glucose which suppresses lipogenesis.</p>
<ol class="tight" data-tight="true"><li><p>Increased anabolic hormone production</p></li><li><p>Inherent anabolic effects of certain fatty acids</p></li></ol><p></p>
<p>androgen receptor</p>
<p>40</p>
<p>weeks and even months</p>
<p>Testosterone acts on androgen receptors, and this information is passed to the muscle cell cores which give instructions to synthesize muscle proteins (genomic effect). Testosterone also aids in the formation of new satellite cells which contribute to myonuclear addition. Without myonuclear addition (increase in muscle cell nuclei) muscle growth is inherently limited as each nucelus as a limited transcriptional capacity.</p>
<ol class="tight" data-tight="true"><li><p>Aids in muscle repair</p></li><li><p>Strengthens bones, joints, and connective tissues</p></li><li><p>Anti-catabolic (prevents muscle damage)</p></li><li><p>Decentralizes body fat distribution (improving metabolic health and causing less fat storage around the midsection)</p></li><li><p>Increases metabolism</p></li></ol><p></p>
<ol class="tight" data-tight="true"><li><p>Anti-inflammatory</p></li><li><p>Improved total cholesterol levels and slightly raising HDL levels</p></li><li><p>Improvement in insulin resistance</p></li><li><p>Improvement in endothelial function</p></li><li><p>Improvement in depression</p></li><li><p>Improvement in thrombosis (blood clots)</p></li><li><p>Improvement in hypertension</p></li><li><p>Improvement in anti-inflammatory joint pain</p></li></ol><p></p>
<p>+700 g; 3 g</p>
<ol class="tight" data-tight="true"><li><p>Lower chronic inflammation levels - which improves acute inflammation signaling to repair damage muscles after training</p></li><li><p>Protect against excessive muscle damage and improve neuromuscular recovery</p></li><li><p>Lower cortisol levels, reducing catabolic activity and improving nutrient partitioning</p></li><li><p>Increase testosterone production</p></li><li><p>Increase anabolic signaling and MPS after meals</p></li><li><p>Increase fat oxidation rates and metabolism by increasing MPS rates and LBM</p></li></ol><p></p>
<p>liver<br>lipoproteins</p>
<p>LDL cholesterol is seen as bad due to the capacity of its load of cholesterol and other lipids to clog up your blood vessels. However, LDLs are vital for lipid metabolism in the body. LDLs are just lipid transporters in the body so they are not inherently unhealthy. </p>
<ol class="tight" data-tight="true"><li><p>LDLs can break or get stuck in our blood vessels, causing cholesterol to clog up the blood vessel.</p></li><li><p>Over time, excessive cholesterol accumulation can cause plaque to build up which narrows the blood vessel and obstructs blood flow.</p></li><li><p>Cholesterol getting stuck in our arteries in the primary cause of cardiovascular disease.</p></li><li><p>When lipids enter our arterial wall, they form plaque which obstructs blood flow - this process is called atherosclerosis.</p></li></ol><p></p>
<p>the total apolipoprotein B (ApoB) particle number</p>
<p>apolipoprotein B (ApoB)</p>
<ol><li><p><span style="color: rgb(255, 255, 255)">ApoB is the primary lipoprotein in chylomicrons, VLDL, IDL, and LDL - each of these has one ApoB particle.</span></p></li><li><p><span style="color: rgb(255, 255, 255)">Total ApoB particle number is a great unified measure for the total non-HDL cholesterol as well as the actual cause of plaque formation.</span></p></li></ol><p></p>
<p><span style="color: rgb(255, 255, 255)">If your diet doesn’t contain much cholesterol, your intestines will increase their absorption to compensate. If that is not enough, your body will produce its own cholesterol. If your diet contains excessive amounts of cholesterol: (i) your body will reduce its absorption, (ii) the liver will decrease its synthesis, and (iii) the cholesterol excretion rate increases. Therefore, for most people, how much cholesterol you eat doesn’t have much effect on how much cholesterol in your blood.</span></p><p></p>
