The Evidence for Low-Fat or Cholesterol Diets Isn't Really There
- Thread starter ☑︎#VoteDemocrat
- Start date
I agree.
Low-fat diets are actually BAD for you, because lack of fat means you'll be hungrier (since fat is satiating) and eating more carbs. The extra carbs will cause blood sugar spikes and make you more likely to gain weight. And cholesterol in food doesn't really affect cholesterol levels in your blood, it has more to do with trans/saturated fat. That's why seafood (which is usually high in cholesterol) is considered heart healthy.
Rather than a low-fat diet, I'd advise people to watch carb intake and not worry about fat.
Low-fat diets are actually BAD for you, because lack of fat means you'll be hungrier (since fat is satiating) and eating more carbs. The extra carbs will cause blood sugar spikes and make you more likely to gain weight. And cholesterol in food doesn't really affect cholesterol levels in your blood, it has more to do with trans/saturated fat. That's why seafood (which is usually high in cholesterol) is considered heart healthy.
Rather than a low-fat diet, I'd advise people to watch carb intake and not worry about fat.
Bernie Madoff
Banned
Vegetarian/Vegan life brehs 
Didn't watch the video but balance and moderation is the key.
my diet typically reflects a High CHO, moderate protein, moderate fat intake meal plan.
I will say that a low carb diet will have people on the verge of committing dat.
let's see what Dr. @POPHOLITDOWN has to say about this
my diet typically reflects a High CHO, moderate protein, moderate fat intake meal plan.
I will say that a low carb diet will have people on the verge of committing dat.
let's see what Dr. @POPHOLITDOWN has to say about this
Sounds like you're not buying biochemistry either
Yuuuuuuuup
All that fructose bypasses normal glycolysis too
But I don't wanna confuse anyone
Malnutrition on account of having moral hangups about being a p*ssy brehsVegetarian/Vegan life brehs
Yuuuuuuuup
All that fructose bypasses normal glycolysis too
But I don't wanna confuse anyone
unnecessary
Bernie Madoff
Banned
yepMalnutrition on account of having moral hangups about being a p*ssy brehs
Cholesterol, Lipoproteins and the Liver
Lipids are transported in the circulation packaged in lipoproteins. The clinical relevance of blood lipid levels is that abnormal levels of lipids in certain lipoproteins are linked to an increase risk of atherosclerosis. Atherosclerosis is a cardiovascular disease in which lipids and inflammatory cells accumulate in plaques within the walls of blood vessels. As a result, vessel walls are narrowed and clots may form, impeding blood flow and oxygen delivery and causing tissue injury. Heart disease occurs because the coronary arteries supplying the heart are a major site where atherosclerotic plaques form.
The liver is central to the regulation of cholesterol levels in the body. Not only does it synthesize cholesterol for export to other cells, but it also removes cholesterol from the body by converting it to bile salts and putting it into the bile where it can be eliminated in the feces. Furthermore, the liver synthesizes the various lipoproteins involved in transporting cholesterol and lipids throughout the body. Cholesterol synthesis in hepatocytes is under negative feedback regulation: increased cholesterol in the cell decreases the activity of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis.
Types of Lipoproteins
Lipoproteins are particles that contain triacylglycerol, phospholipids and cholesterol and amphipathic proteins called apolipoproteins. You can refresh your memory about the structure of lipoproteins by visiting the web page from fall quarter. Lipoproteins can be differentiated on the basis of their density, but also by the types of apolipoproteins they contain. The degree of lipid in a lipoprotein affects its density—the lower the density of a lipoprotein, the more lipid it contains relative to protein. The four major types of lipoproteins are chylomicrons, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL).
The figure below summarizes the fates of lipoproteins produced by the liver. Refer to it as you read about the different lipoproteins.
Disorders and Drug Treatments
The link between cholesterol and heart disease was recognized through the study of individuals with familial hypercholesterolemia. Individuals with this disorder have several-fold higher levels of circulating LDL due to a defect in the function of their LDL receptors. Without functioning LDL receptors, LDL is not cleared from the circulation. As well, because cholesterol cannot get into cells efficiently, there is no negative feedback suppression of cholesterol synthesis in the liver.
A lipid profile typically measures the levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. Dyslipidemia is the term that is used if lipid levels are outside the normal range. High levels of LDL cholesterol (the so-called “bad cholesterol”) greatly increase the risk for atherosclerosis because LDL particles contribute to the formation of atherosclerotic plaques. Low HDL levels ("good cholesterol") are an independent risk factor, because reverse cholesterol transport works to prevent plaque formation, or even cause regression of plaques once they have formed. HDL may also have anti-inflammatory properties that help reduce the risk of atherosclerosis. Fasting triglyceride levels are used to estimate the level of VLDL. High levels of triglycerides are also associated with an increased risk for atherosclerosis, although the mechanism is not entirely clear.
The most important drugs for the treatment of dyslipidemia are by far, the statins. Statins have been shown in multiple clinical trials to reduce cardiovascular events and mortality.
The drugs below are used to treat dyslipidemia in specific subsets of patients.
Lipids are transported in the circulation packaged in lipoproteins. The clinical relevance of blood lipid levels is that abnormal levels of lipids in certain lipoproteins are linked to an increase risk of atherosclerosis. Atherosclerosis is a cardiovascular disease in which lipids and inflammatory cells accumulate in plaques within the walls of blood vessels. As a result, vessel walls are narrowed and clots may form, impeding blood flow and oxygen delivery and causing tissue injury. Heart disease occurs because the coronary arteries supplying the heart are a major site where atherosclerotic plaques form.
The liver is central to the regulation of cholesterol levels in the body. Not only does it synthesize cholesterol for export to other cells, but it also removes cholesterol from the body by converting it to bile salts and putting it into the bile where it can be eliminated in the feces. Furthermore, the liver synthesizes the various lipoproteins involved in transporting cholesterol and lipids throughout the body. Cholesterol synthesis in hepatocytes is under negative feedback regulation: increased cholesterol in the cell decreases the activity of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis.
Types of Lipoproteins
Lipoproteins are particles that contain triacylglycerol, phospholipids and cholesterol and amphipathic proteins called apolipoproteins. You can refresh your memory about the structure of lipoproteins by visiting the web page from fall quarter. Lipoproteins can be differentiated on the basis of their density, but also by the types of apolipoproteins they contain. The degree of lipid in a lipoprotein affects its density—the lower the density of a lipoprotein, the more lipid it contains relative to protein. The four major types of lipoproteins are chylomicrons, very low-density lipoprotein (VLDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL).
The figure below summarizes the fates of lipoproteins produced by the liver. Refer to it as you read about the different lipoproteins.
- Chylomicrons and VLDL deliver TAG to cells in the body. Two types of lipoproteins are triglyceride-rich: the chylomicrons and VLDL. Chylomicrons are synthesized by enterocytes from lipids absorbed in the small intestine. VLDL is synthesized in the liver. The function of these lipoproteins is to deliver energy-rich triacylglycerol (TAG) to cells in the body (pink pathway). TAG is stripped from chylomicrons and VLDL through the action of lipoprotein lipase, an enzyme that is found on the surface of endothelial cells. This enzyme digests the TAG to fatty acids and monoglycerides, which can then diffuse into the cell to be oxidized, or in the case of an adipose cell, to be re-synthesized into TAG and stored in the cell.
- LDL delivers cholesterol to cells in the body. As VLDL particles are stripped of triacylglycerol, they become more dense. These particles are remodeled at the liver and transformed into LDL. The function of LDL is to deliver cholesterol to cells, where it is used in membranes, or for the synthesis of steroid hormones (blue pathway). Cells take up cholesterol by receptor-mediated endocytosis. LDL binds to a specific LDL receptor and is internalized in an endocytic vesicle. Receptors are recycled to the cell surface, while hydrolysis in an endolysosome releases cholesterol for use in the cell.
- HDL is involved in reverse cholesterol transport. Excess cholesterol is eliminated from the body via the liver, which secretes cholesterol in bile or converts it to bile salts. The liver removes LDL and other lipoproteins from the circulation by receptor-mediated endocytosis. Additionally, excess cholesterol from cells is brought back to the liver by HDL in a process known as reverse cholesterol transport (green pathway). HDL (or really, the HDL precursor) is synthesized and secreted by the liver and small intestine. It travels in the circulation where it gathers cholesterol to form mature HDL, which then returns the cholesterol to the liver via various pathways.
Disorders and Drug Treatments
The link between cholesterol and heart disease was recognized through the study of individuals with familial hypercholesterolemia. Individuals with this disorder have several-fold higher levels of circulating LDL due to a defect in the function of their LDL receptors. Without functioning LDL receptors, LDL is not cleared from the circulation. As well, because cholesterol cannot get into cells efficiently, there is no negative feedback suppression of cholesterol synthesis in the liver.
A lipid profile typically measures the levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. Dyslipidemia is the term that is used if lipid levels are outside the normal range. High levels of LDL cholesterol (the so-called “bad cholesterol”) greatly increase the risk for atherosclerosis because LDL particles contribute to the formation of atherosclerotic plaques. Low HDL levels ("good cholesterol") are an independent risk factor, because reverse cholesterol transport works to prevent plaque formation, or even cause regression of plaques once they have formed. HDL may also have anti-inflammatory properties that help reduce the risk of atherosclerosis. Fasting triglyceride levels are used to estimate the level of VLDL. High levels of triglycerides are also associated with an increased risk for atherosclerosis, although the mechanism is not entirely clear.
The most important drugs for the treatment of dyslipidemia are by far, the statins. Statins have been shown in multiple clinical trials to reduce cardiovascular events and mortality.
- Statins
These drugs inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. They are designed to mainly inhibit the enzyme in the liver. Inhibition of cholesterol synthesis further decreases circulating LDL because reduced levels of cholesterol in the hepatocyte cause it to upregulate expression of LDL receptors.
The drugs below are used to treat dyslipidemia in specific subsets of patients.
- Fibrates
Fibrates bind to the nuclear receptor PPAR-alpha. This receptor works as a transcription factor to alter gene expression in target cells. Fibrates increase HDL levels and decrease triglyceride levels. Fibrates are primarily used when the primary problem is high levels of triglycerides.
- Niacin (Nicotinic Acid)
You may know of niacin as an essential nutrient of the vitamin B complex. At high doses (much higher than required for its role as a vitamin), niacin increases HDL levels and decreases triglyceride and LDL levels. The mechanism of action of niacin is not fully defined, but it appears to inhibit an enzyme in the liver that is involved in triacylglycerol synthesis, causing a decrease in VLDL production. Another effect in the liver is to prolong the half-life of HDL particles by preventing HDL breakdown. Recent work has also identified a specific receptor for niacin that may also play a role in mediating its action. Niacin is indicated when HDL is low, as it is the most effective drug for raising HDL levels.
- Ezetimibe
Ezetimibe inhibits cholesterol absorption in the small intestine. This reduces absorption of dietary cholesterol, but also promotes cholesterol excretion, since biliary cholesterol accounts for some of the cholesterol that passes through the small intestine. Ezetimibe effectively lowers LDL cholesterol, however clinical trials have called into question whether further lowering cholesterol with this drug is truly beneficial in reducing atherosclerotic plaque. The most recent results of a large clinical trial testing the combination of ezetimibe with a statin (IMPROVE-IT trial) has shown that is has a modest benefit in reducing heart disease.
POPHOLITDOWN
Mama I love you.
Didn't watch the video but balance and moderation is the key.
my diet typically reflects a High CHO, moderate protein, moderate fat intake meal plan.
I will say that a low carb diet will have people on the verge of committing dat.
let's see what Dr. @POPHOLITDOWN has to say about this
Bruh,,,the cholesterol hypothesis is a farce my nikka
There is an over abundance of evidence that demonstrates that cholseteral intake has literally NOTHING to do with your chloesterola levels...
There was an article this week by a fairly respectable doc at UCSD sbout this...however, he was definitely promoting his vegan agenda....but he quoted some of the big papers that recently suggest that choletesterol intake reslly has more to do with GENETICS and relative calorie intake than nething else
Im a surgeon so I dont give a fukk about ppls lifestyles as long as they want they bones fixed....buuuuuut if a nikka wanted my advice ona lifestyle choice...
i would SAY EVERYTHING IN MODERATION....I eat 300 grams of protein a day and work 7 days a weel with an emphasis on BENCh/SQUATS/DEADLIFT...i kno 300 is prolly OD and ive seen the reasearch but i keep a diet that is maintanable for me and keep a Kobe mindset and I dont take any mind altering meds other than etOH and the occaasional indica
im a big nikka tho so i kno my shyt aint for everyone
Its really funny on the low end. Cholesterol can't be fukked with...all you can do is throw statins at the shytBruh,,,the cholesterol hypothesis is a farce my nikka
There is an over abundance of evidence that demonstrates that cholseteral intake has literally NOTHING to do with your chloesterola levels...
There was an article this week by a fairly respectable doc at UCSD sbout this...however, he was definitely promoting his vegan agenda....but he quoted some of the big papers that recently suggest that choletesterol intake reslly has more to do with GENETICS and relative calorie intake than nething else
Im a surgeon so I dont give a fukk about ppls lifestyles as long as they want they bones fixed....buuuuuut if a nikka wanted my advice ona lifestyle choice...
i would SAY EVERYTHING IN MODERATION....I eat 300 grams of protein a day and work 7 days a weel with an emphasis on BENCh/SQUATS/DEADLIFT...i kno 300 is prolly OD and ive seen the reasearch but i keep a diet that is maintanable for me and keep a Kobe mindset and I dont take any mind altering meds other than etOH and the occaasional indica
im a big nikka tho so i kno my shyt aint for everyone