Hmmm... I found this and it made me wonder.
Bad cholesterol is typically found in animal-based products: meats and dairy. This is yet another reason to avoid them, and why doctors suggest sticking to a plant-based diet.
See, I know that "meats and dairy", in particular dark meats and milk, contain sugars that increase the bacterial populations and that might be related to cholesterol. Perhaps these sugars tax the liver just like sucrose/fructose?
So, the question becomes... does saturated fat and cholesterol consumption increase cholesterol?
A good food for this would be cheese. It's both high in saturated fat and cholesterol, extremely low in sugar and high in "probiotics".
I already looked and I remember it finding no assocation between cheese consumption and cholesterol.
So, obviously "meats and dairy" is too broad of a label. It should be, more or less, meats and dairy with sugars, which milk and dark meats have plenty of. How exactly these sugars caused increase cholesterol levels, either via bacteria or via the liver, I don't exactly know but I highly suspect it's one of the two. I know that fructose/sucrose consumption vastly increases cholesterol, but glucose doesn't, and bacteria can readily metabolize glucose/sucrose/fructose, so that suggests that milk and dark meats tax the liver with their sugars, which itself causes high cholesterol. I just didn't know that meat sugars were essentially fructose? Maybe they're not... and maybe the liver metabolizes more than just fructose... or maybe it is... and meat sugars are essentially sucrose or one of its homologs, which gets broken down into fructose in the digestive tract. I'd have to look more into meat sugars. Let's look into milk. It's sugars...
Sucrose - made up of fructose and glucose.
Lactose - made up of galactose and glucose.
Galactose - apparently the same as glucose/fructose - C6H12O2. So one of the three 'essential sugars'. Does the liver metabolize galactose? Because... obviously... cells use glucose and not galactose... so it gets converted somewhere...now the question is where...
https://en.wikipedia.org/wiki/Galactose#Metabolism
The main pathway of galactose metabolism is the Leloir pathway; humans and other species, however, have been noted to contain several alternate pathways, such as the De Ley Doudoroff pathway.
So what organ is responsible for this pathway?
The Leloir pathway consists of the latter stage of a two-part process that converts β-D-galactose to UDP-glucose. The initial stage is the conversion of β-D-galactose to α-D-galactose by the enzyme, mutarotase (GALM). The Leloir pathway then carries out the conversion of α-D-galactose to UDP-glucose via three principal enzymes: Galactokinase (GALK) phosphorylates α-D-galactose to galactose-1-phosphate, or Gal-1-P; Galactose-1-phosphate uridyltransferase (GALT) transfers a UMP group from UDP-glucose to Gal-1-P to form UDP-galactose; and finally, UDP galactose-4’-epimerase (GALE) interconverts UDP-galactose and UDP-glucose, thereby completing the pathway.
Not much clues there.
https://en.wikipedia.org/wiki/Leloir_pathway
The Leloir pathway is a metabolic pathway for the catabolism of D-galactose. It is named after Luis Federico Leloir.
In the first step, galactose mutarotase facilitates the conversion of β-D-galactose to α-D-galactose since this is the active form in the pathway. Next, α-D-galactose is phosphorylated by galactokinase to galactose 1-phosphate. In the third step, D-galactose-1-phosphate uridylyltransferase converts galactose 1-phosphate to UDP-galactose using UDP-glucose as the uridine diphosphate source. Finally, UDP-galactose 4-epimerase recycles the UDP-galactose to UDP-glucose for the transferase reaction. Additionally, phosphoglucomutase converts the D-glucose 1-phosphate to D-glucose 6-phosphate.[2][3]
No clues there.
Let's look into this galactose metabolism disorder... perhaps we can infer what organs are involved.
In individuals with galactosemia, the enzymes needed for further metabolism of galactose are severely diminished or missing entirely, leading to toxic levels of galactose 1-phosphate in various tissues as in the case of classic galactosemia, resulting in hepatomegaly (an enlarged liver), cirrhosis, renal failure, cataracts, vomiting, seizure, hypoglycemia, lethargy, brain damage, and ovarian failure
ok, seeing liver and kidney affects here. Suggests it's one of those or both...
Well, I give up. Can't find anyone explaining what organs are involved in this process, but there's high suspicion that the liver mediates the conversion between galactose to glucose, just like it mediates the conversion between fructose to glucose. This suggests then that galactose consumption taxes the liver.
All 3 sugars in milk, then, directly tax the liver. Cheese, where the sugars have been metabolized by bacteria, would not tax the liver. So, that explains the different affects between mlik and cheese in cholesterol levels. All3 sugars in milk tax the liver, whereas cheese has no sugar to tax the liver, so milk increases cholesterol while cheese has no affect. Does the research bear this out? That milk consumption causes increased cholesterol?
This article, http://www.livestrong.com/article/267670-does-milk-raise-cholesterol-levels/, implies that milk causes increased cholesterol, but it wrongly assumes it's because of the saturated fat. That's a common mistaken belief. (Cheese, which is ultra high in saturated fat and cholesterol, has no affect on serum cholesterol.)
It's interesting, I can't seem to find much research on milk consumption and serum cholesterol. It seems that milk possibly gets generalized into "dairy" all the time, which is a bad generalization to make. Cheese is nothing like milk, in terms of its health affects and affects on bacteria. Maybe I'm just not using the 'right' key words...
Well this research paper is also looking in the wrong direction...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926059/
Milk contains a large number of bioactive compounds, but milk fat has the largest impact on plasma lipids. The lipid pattern in dairy fat is very complicated and more than 400 different fatty acids have been identified. About 70% of dairy fat contains SFAs of which the majority (45%) are of 12–16 carbon chain length and 2.7% are tFAs (13), and these have the ability to raise plasma cholesterol. Except for the concentration of different types of plasma lipoproteins that can be affected, their size and composition will change in response to different types of dietary fat. For example, it is suggested that larger sizes of lipoproteins are less atherogenic than smaller sizes (25) and some of the fatty acids typically found in milk fat have been associated with less dense LDL particles (26).
Other milk components like proteins, calcium, and lactose have been suggested to affect lipid metabolism directly or indirectly, but the strongest impact on plasma lipids emerges from the intake of milk fat.
But, it does highly suggest that milk consumption does increases cholesterol. They fail the notice that cheese does not, which negates the 'saturated fat' causal hypothesis and, in my opinion, puts sole focus on the milk sugars. Not just lactose, but all three sugars - sucrose, galactose and lactose - which all more-than-likely get metabolized by the liver in the eventual conversion to glucose.
To recap, the liver metabolizes fructose and galactose, but not glucose. That suggests that glucose and the starches (Which gets broken down into glucose by amylase) are the sole foods/carb-types in the carbohydrate family that don't tax the liver. Everything else does. Fruits, milk, meat, anything with sugars. Obviously, the more milk/meat/fruit you eat, the more the liver gets taxed.
I wonder...
if high fruit consumption is associated with liver failure... or 'fatty liver'... maybe it doesn't for some special reason...
Seeing a lot of articles suggesting fruit to 'heal up' fatty liver. But, they are definitely not research articles, so I don't put much credence into that. The "common understanding" seems to be commonly looking at and focusing on the wrong suspect, and making many false assumptions in the process, like possibly... "Fruit heals up livers.". Not saying it's false, but not seeing a lot of clinical evidence that its true. So far, I've found no clinical evidence.
Mean daily intake of total, industrial and fruit fructose was 18.0±8.7g, 6.0±4.7g, and 11.9±7.2g, respectively. Intake of industrial, not fruit fructose, was independently associated with higher WHR (p=0.02) and hypercaloric diet (p<0.001). CHC patients with severe liver fibrosis (⩾F3) reported a significantly higher intake of total (20.8±10.2 vs. 17.2±8.1g/day; p=0.04) and industrial fructose (7.8±6.0 vs. 5.5±4.2; p=0.01), not fruit fructose (12.9±8.0 vs. 11.6±7.0; p=0.34). Multivariate logistic regression analysis showed that older age (OR 1.048, 95% CI 1.004-1.094, p=0.03), severe necroinflammatory activity (OR 3.325, 95% CI 1.347-8.209, p=0.009), moderate-severe steatosis (OR 2.421, 95% CI 1.017-6.415, p=0.04), and industrial fructose intake (OR 1.147, 95% CI 1.047-1.257, p=0.003) were independently linked to severe fibrosis. No association was found between fructose intake and liver necroinflammatory activity, steatosis, and the features of NASH.
Hmmm... doesn't seem conclusive... but it is highly suggestive that fruit doesn't cause liver damage. So, there is something special about fruit that doesn't tax the liver as much as dark-meat/milk/sucrose/fructose does. And, I don't actually know if dark-meat/milk taxes the liver, I just assume it does because of its known affects on serum cholesterol, and the known connection between the liver and cholesterol(The liver produces cholesterol), and the fact that milk/dark-meat have sugars that get metabolized by the liver, and fructose/sucrose causes increased cholesterol but glucose does not. Seems like those facts suggests milk/dark-meat taxes the liver. Since there's a connection between liver and heart health, that would imply milk and dark meat consumption is associated with CVD (Which it is according to research) whereas whole fruit consumption does not (Which, according to that food/CVD data table I earlier linked, it does not.). So, this implies that the liver is a mediator between food consumption and heart health. It seems like Staph Aureus is too... seems like there's a lot of mediators in heart health... lungs, liver, staph aureus in the digestive tract, vessel diameter as a function of exercise/physical-activity... which only makes sense... It's tied to so many different systems. The brain could also be tied to heart health... which seems to be. Yes, so many different mediators.
I do highly believe, though, artersclerosis is caused solely by Staph Aureus. But, arthersclerosis is but one mediator of "heart health" (An important one in many cases, but not the only one.). patent vessel diameter isn't just a function of arthersclerosis, but also of vessel diamater, which appears to be a function of exercise, stress/cortisol and food consumption (Less food consumption = cortisol = vasoconstriction. In the longterm, vessel shrinkage. Microvascular issues are common among anorexics.).
In regards to diet, it's important to eat enough (it's better to eat too much, than not enough) and it's important to eat "good food".
In regards to the liver, I actually don't know the exact relationship between the liver and heart. I.e., how a damaged/fatty liver could cause heart problems.
Growing evidence suggests there's a strong link between NAFLD and dangerous plaque inside the heart's arteries. The inflammatory compounds and other substances pumped out by a fat-afflicted liver might promote the atherosclerotic process that damages the insides of arteries and makes blood more likely to clot. This combination may lead to a heart attack or a stroke.
Hmmm... since there's an association between NAFLD and arthersclerosis, maybe there's an association between staph aureus and fatty liver...
https://www.ncbi.nlm.nih.gov/pubmed/20492505
Staphylococcus aureus increasingly is recognized as an important pathogen in patients with chronic liver diseases. The purpose of this study was to evaluate clinical features and the outcome of S. aureus infections in patients with chronic liver diseases.
Oh, interesting, staph aureus is thought to cause chronic liver disease. Seems like there''s a high likelihood of an association between staph aureus and fatty liver.
What does a "fatty liver" look like? Does it look anything like pimples, athersclerotic plaques, or impetigo?
Searching google images...
Interesting...
Lemon is a known strong antibiotic, and it's thought to treat fatty liver... does suggest staph aureus causes fatty liver...
Here's a fatty liver...
Oh, look, yellow/white spots... has the yellow/whiteness in pimples and arthersclerotic plaques and the spottiness of impetigo and the 'staph aureus' skin diseases (Carbunkles,boils,etc.). Maybe normal healthy livers have bumps?
No, definitely no bumps and no yellow/white spots. Hmm... this is strongly suggestive that the spots in the "fatty liver" are essentially staph aureus infections. Which, it's already been implicated in chronic liver disease, so this is an extremely strong possibility.
Yep, so staph aureus causes fatty liver AND arthersclerosis. That's the link between liver and heart health. [Not this 'inflammatory compounds' jazz. That's a byproduct of infection, not a cause of the infections' outcomes, like heart disease.)
I wonder if that's why fruit consumption isn't linked to liver damage. It's already explained in my peak bacterial population equation I posted earlier... that equation suggests that the peak staph aureus colony size after consuming a whole fruit would be minimal compared to higher density sugar sources... and that explains the lack of association between liver problems and whole fruit consumption, despite the fact it contains sucrose/fructose. So liver problems = bacteria, not necessarily fructose/sucrose. This would imply that if fructose/sucrose increases cholesterol through the liver, than cholesterol by itself has little causal association with liver damage or heart health, though there might /seem/ to be an association through refined/processed fructose/sucrose containing food consumption. Indeed, that one food/CVD table I posted earlier showed an inverse association between total cholesterol and CVD risk. So...
-Sucrose/Fructose/Galactose causes cholesterol through liver metabolism.
-Cholesterol is not a cause of heart disease. There'd be a statistical association via the connection between refined sucrose/fructose/galactose/glucose consumption and bacteria growth, but not a causal relationship. (That is to say, some forms of "high cholesterol" might be associated with heart disease, but it's not causing it, the bacteria is. Cholesterol is an irrelevant byproduct of liver metabolism.)
-Staph auerues is both a cause of fatty liver and liver disease as well as some common forms of heart disease (Like, arthersclerosis and blockages).
-Consumption of refined carbs, including fructose/sucrose containing ones(candy) and glucose containing ones(refined starches like bread,cracker,setc.), is a cause of staph aureus and thus liver & heart disease. Fibrous unrefined carbs, like Bananas and most fruits, are not a major cause of staph aureus and thus heart disease. I do wonder if excess fruit consumption would be associated with staph aureus colonies... if it has a minor growth affect, then excess consumption might have a 'major' growth affect. Seems if you drink too much coconut water, like I did, you get too much fructose which then causes excess bloating, suggesting high bacteria growth. It then seems possible to growth staph aureus colonies through excess fruit consumption... but .... coconut water isn't exactly a fibrous fruit. The question is about excessive fibrous fruit consumption... not juices...
So, have I ever felt sick to my stomach from eating too much fibrous fruit... nope... can't say that I have...
That's not true of too much sugar. Oh, it's pretty easy to get sick to your stomach from eating too much candy.