The 5 Ss of Xenoestrogen Warfare

"Bad cholesterol hypothesis" is a discredited pseudo scientific fraud propped up by pharmaceuticals who're pushing with malicious of forethought a useless, dangerous, contra-indicated poison called statin medication.

Dispelling pseudo scientific notions

(a) Cholesterol in your blood is largely put there by the liver, 70-80% and is maliciously controlled by it, because the liver regulates energy metabolism in humans
(b) Cholesterol is a composite of every cell in your body by 50%, brain 50-70%, nervous system 70%+
(c) Cholesterol is an enzymatic precursor to a ton of important reactions, ie testosterone, immune function, etc
(d) lipo-protein carriers(LDL) shuttle nutrients into the body and are essential for normal human physiological functioning, again where the liver determines the level as based on need
(e) if you grew up with Mevalonate Kinase Deficiency(MKD) which statins mimic by disabling cholesterol metabolism in humans, you'd have grown up deformed and your muscles atrophied
(f) 20% of statin users suffer severe and adverse reactions, unsurprisingly

Where the pseudo scientists lie out the mouth

(a) LDL is not causal of Cardiovascular disease
(b) native LDL cannot cause nor create metabolic disorders in the body
(b) LDL has to be damaged by inflammatory processes, oxidative processes
(e) saturated animal fat is not conducive because its the most resistant to oxidization, inflammation, this also includes coconut oil and olive oil(virgin pressed)
(f) polyunstaturated and trans-fats are extremely prone to oxidization, eating them chronically will also alter your body's omega 3 to 6 ratios making your body more prone to inflammation and oxidization
(e) junk food is cancerous for this reason, sugary junk foods, fruit, cereals, chips, deep fried shit, peanut butter, etc etc
(f) meta-analysis of statin clinical intervention to effect the government recommended "low LDL, high HDL" profile was found to have no impact on cardiovascular disease. In fact those with lower LDL did worse in mortality against those with higher LDL levels.
(g) the cholesterol hypothesis, is still a hypothesis after decades because all the "supporting literature" is associative data, epidemiological. For those new to research statistics, associations cannot infer causality. Why? Because associations are uncontrolled variables and they do not control for confounders. In order for something to be established as causal it must meet the 9-10 or so Bradford Hill criteria. What else is associative? Conspiracy theories. This is why associative data is almost weighted at the very bottom of the "hierarchy of evidence", just above "expert testimony". What is needed is a "mechanism", a known and established way the body works to underpin disease progression(pathophysiology). The known mechanisms do not support the bad cholesterol hypothesis.

What are the causal variables of inflammation, oxidization from diet?

(a) carbohydrate(sugar)
(b) combing carbs with fats in any equivalence creates the most insulinogenic, inflammatory response possible from diet, detailed in a human physiological mechanism called "The Randle Cycle"
(c) "The Randle Cycle" details in another way the most efficient way in human physiology to gain body fat because it has the strongest effect on insulin
(d) sugar spikes blood glucose levels also causing glycation, which occurs from eating carbohydrate foods, which again makes the body heavily susceptible to inflammation and oxidization
(e) Diabetes Mellitus pathophysiology Quote - "Diabetes mellitus (DM) is a group of diseases characterized by a disrupted carbohydrate metabolism leading to elevated blood glucose levels (= hyperglycemia) and secretion of glucose in the urine (= glycosuria) as a result of insufficient production or functioning of the pancreatic hormone insulin, combined with a number of yet undefined predisposing factors. DM is not a pathogenic entity but a group of etiologically different metabolic defects. Chronic hyperglycemia causes long-term damage, dysfunction and failures of various cells, tissues and organs."

Guess the composite of the government recommended "Standard American Diet"? Those fucking cock suckers are purposefully trying to poison us, then reap our rotting bodies with useless pharmaceuticals which do not treat root causation, but are purely for medicating symptoms.

Second thing to note, carbohydrates are fat storing and not used effectively for energy. Its the total opposite for fat. This is beared out in all recent isocaloric studies in metabolic wards where people on high fat diets have a metabolic advantage over high carb dieters. The reason as should be obvious by now, the body loves to use fat for energy.

In terms of diabetes fat is the least insulinogenic food known. Meat also doesn't even register on the glycemic load index because it has almost no carbohydrates in them. Its almost impossible to create a diabetic from someone who eats unprocessed animal meat, fat, organs.

Edit:1 (some edits, more links to literature)

The only benefit of statins seems to be their anti-inflammatory effect which is entirely by random chance, as it was never planned for when statins were originally developed... An effect that can be safely mediated with other interventions rather than this dangerous, contra-indicated poison.

Statins inhibit the enzyme HMG-CoA reductase, at a stage early in the mevalonate pathway.10 This pathway generates a range of other products in addition to cholesterol, such as coenzyme Q10, heme-A, and isoprenylated proteins,10 which have pivotal roles in cell biology and human physiology and potential relevance to benefits as well as risks of statins.11-13 Additionally, cholesterol itself is not merely a final product (with its own range of vital roles) but also an intermediate to a suite of additional products of fundamental relevance to health and well-being, such as sex steroids, corticosteroids, bile acids and vitamin D, several of which have been shown to be affected with statin administration.14, 15 The biochemical influences of statins extend well beyond the lipid profile and its constituents (low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides), and even beyond the direct products of the mevalonate pathway, to include a wide swath of products and functions modified through these as well as nonmevalonate effects of statins, ranging from nitric oxide and inflammatory markers16 to polyunsaturated fatty acids,17 among many others.

Source: Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism

Quick note, Mevalonate Kinase Deficiency(MKD) can be stimulated specifically by blocking the Mevalonate Pathway via statin drugs.

Furthermore, statins are used as a pharmacological compound to biochemically reproduce some features of Mevalonate Kinase Deficiency (MKD)—a pathology characterized by a defect in a key enzyme of mevalonate pathway [13,25,26]. In some studies, mevalonate pathway blockade, obtained in neuronal and monocytic cell lines by statin (Lovastatin) administration, induces an increase of apoptosis correlated to mitochondrial damage [27,28,29].

The more severe effect of (MKD) and is labaled as mevalonic aciduria (MVA).

People with MVA have signs and symptoms of the condition at all times, not just during episodes of fever. Affected children have developmental delay, problems with movement and balance (ataxia), recurrent seizures (epilepsy), progressive problems with vision, and failure to gain weight and grow at the expected rate (failure to thrive). Individuals with MVA typically have an unusually small, elongated head. In childhood or adolescence, affected individuals may develop eye problems such as inflammation of the eye (uveitis), a blue tint in the white part of the eye (blue sclera), an eye disorder called retinitis pigmentosa that causes vision loss, or clouding of the lens of the eye (cataracts). Affected adults may have short stature and may develop muscle weakness (myopathy) later in life. During fever episodes, people with MVA may have an enlarged liver and spleen (hepatosplenomegaly), lymphadenopathy, abdominal pain, diarrhea, and skin rashes. Children with MVA who are severely affected with multiple problems may live only into early childhood; mildly affected individuals may have a normal life expectancy.

Cannot stress enough how much statins are a dangerous, useless, contra-indicated poison.

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[–]3Yakatonker0 points1 point2 points 6 years ago* (0 children) | Copy Link

Have you ever googled "Cholesterol metabolism" and looked up where statins disable the fatty acid reactive chain? They kill an enzymatic precursor that's used to power an innumerable physiological processes in the body.

Quick note, Mevalonate Kinase Deficiency(MKD) can be stimulated specifically by blocking the Mevalonate Pathway via statin drugs.

Furthermore, statins are used as a pharmacological compound to biochemically reproduce some features of Mevalonate Kinase Deficiency (MKD)—a pathology characterized by a defect in a key enzyme of mevalonate pathway [13,25,26]. In some studies, mevalonate pathway blockade, obtained in neuronal and monocytic cell lines by statin (Lovastatin) administration, induces an increase of apoptosis correlated to mitochondrial damage [27,28,29].

The more severe effect of (MKD) and is labaled as mevalonic aciduria (MVA).

People with MVA have signs and symptoms of the condition at all times, not just during episodes of fever. Affected children have developmental delay, problems with movement and balance (ataxia), recurrent seizures (epilepsy), progressive problems with vision, and failure to gain weight and grow at the expected rate (failure to thrive). Individuals with MVA typically have an unusually small, elongated head. In childhood or adolescence, affected individuals may develop eye problems such as inflammation of the eye (uveitis), a blue tint in the white part of the eye (blue sclera), an eye disorder called retinitis pigmentosa that causes vision loss, or clouding of the lens of the eye (cataracts). Affected adults may have short stature and may develop muscle weakness (myopathy) later in life. During fever episodes, people with MVA may have an enlarged liver and spleen (hepatosplenomegaly), lymphadenopathy, abdominal pain, diarrhea, and skin rashes. Children with MVA who are severely affected with multiple problems may live only into early childhood; mildly affected individuals may have a normal life expectancy.

Hmm, strange, its almost like statins are a dangerous, useless, contra-indicated poison of the highest order? Its not shocking whatsoever when a minimal of 20% of statin users suffer severe and adverse side effects.

The only benefit of statins seems to be their anti-inflammatory effect which is entirely by random chance, as it was never planned for when statins were originally developed... An effect that can be safely mediated with other interventions rather than this contra-indicated poison.

Edit:1 Additional Literature Review of Statin's poisonous effects:

Statins inhibit the enzyme HMG-CoA reductase, at a stage early in the mevalonate pathway.10 This pathway generates a range of other products in addition to cholesterol, such as coenzyme Q10, heme-A, and isoprenylated proteins,10 which have pivotal roles in cell biology and human physiology and potential relevance to benefits as well as risks of statins.11-13 Additionally, cholesterol itself is not merely a final product (with its own range of vital roles) but also an intermediate to a suite of additional products of fundamental relevance to health and well-being, such as sex steroids, corticosteroids, bile acids and vitamin D, several of which have been shown to be affected with statin administration.14, 15 The biochemical influences of statins extend well beyond the lipid profile and its constituents (low-density lipoprotein cholesterol [LDL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides), and even beyond the direct products of the mevalonate pathway, to include a wide swath of products and functions modified through these as well as nonmevalonate effects of statins, ranging from nitric oxide and inflammatory markers16 to polyunsaturated fatty acids,17 among many others.

Source: Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism

I'm not joking when I say this is a very contra-indicated poison.

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Cholesterol Games - Malcom Kendrick

Bart Kay - Nutrition Science Watchdog - Statins might KILL YOU!

Dr. Jason Fung - Intensive Dietary Management (IDM) program

Bart Kay is a former senior lecturer of Cardiovascular and Sleep sciences from the UK, who also served as a peer reviewer for several journals. Dr. Malcom Kendrick also has a background in doing research, and is an outspoken critic of the "bad" cholesterol hypothesis. Both of these men produce ample materials related to their specialization. Bart though talks a bit more about the bastardization of research and the current "publish or parish" paradigm that has researchers out there as glorified whores. Dr. Jason Fung in particular is a nephrologist who's become somewhat of a specialist with weight loss, especially due to his understanding of human physiological mechanisms.

The rest of my understanding involves going into the research literature myself and trying to figure things out. Mainly looking for inconsistencies and trying to establish known biological mechanisms, versus say, correlative-associative studies which are often shilled as "evidence"...

One of those lines I'm pursuing involves the myth of "Blue Zones".

Blue Zones Dietary Myth

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Carbohydrate because it rails on insulin which down regulates a physiological process called gluconeogenesis, the metabolic pathway for converting body fat to energy reduces TEE(total energy expenditure). What happens when you cannot effectively use body fat? Obviously you effect a physiological effect more towards for fat storing.

Does this also show up in metabolic ward studies in carbohydrate versus say ketogenic high fat diets? Yes, keto high fat eaters had a significant metabolic advantage because?

(a) they're not sabotaging human physiology, reducing their energy expenditure
(b) carbohydrates are fat storing because sugar rails efficiently on insulin
(c) sugar also feeds into a vicious reciprocal feed back with increased hunger, lacking satiety because of the crash in blood sugar from insulin
(d) sugar is the most effective way to turn people into fat food addicts

energy balance level

This is a discredited pseudo scientific concept, ie CICO. Why? Because there's not one human physiological mechanism to the thing. The body is not a linear energy system, rather the body itself is a mediator based on "energy in" and can and does effect "energy out" based on things such as the energy sub-straits consumed, fat or carbohydrate(sugar), nutrient timing, etc.

Its pseudo scientific theory pushed by crap food corporations as way to mitigate massive liabilities from peddling toxic food items.

[–]Sumsar01-1 points0 points1 point 6 years ago (4 children) | Copy Link

Look dude the fact that you even link to a single study show me you dont get this stuff. Keto is just a way of eating and it has lower adherance than a normal mediteranian diet and will lower performance at least in resistance training. Any diet will downregulate my energy expenditure, but who gives a fuck it will be back up after week og maintaince and it wont be significant anyways since im not trying to compete in a bodybuilding show. I also already have to eat more than i want to, just to maintain. And yes it is just energy in energy out. It once again shows that you don't get this stuff, the energy balance cant be anything else because of physical laws. It might be a complex function of cercumstance but it's still just energy conservation. There is also a reason why we use approximations, because they are good enough and the real process is to hard/not efficient to describe.

[–]3Yakatonker0 points1 point2 points 6 years ago* (3 children) | Copy Link

mediteranian diet and will lower performance at least in resistance training

The "Mediterranean diet" is not even a scientifically verified diet, its origination was from a special insert that avoided peer review in the American Journal of Nutrition. The back story of which the nutritional habits of the "Mediterranean" lacked anything close to a valid collation of data. It was severely fragmented and was hacked together by special interests and food corporations. If it was peer reviewed in its times, it would've been torn apart under scrutiny which it should've been.

Keto is just a way of eating and it has lower adherance than a normal mediteranian diet

No data to support this inference whatsoever.

will lower performance at least in resistance training

This is confounded because it takes a period of time to become "fat adapted". Most who don't know anything about physiology fail to understand the gut biome also changes in response to diet and the microbes for certain foods increase, decrease based on inputs. Its theorized given metabolic ward studies so far are 40 days, after a high carb intake, the high fat dieters become incredible fat burners. This is not surprising because human biology, the known mechanisms show the body prefers to use fat for energy. We have an unlimited bandwidth for fat as far as there is fat adipose tissue where as this bandwidth doesn't exist for carbohydrate(sugar) or even amino acids(protein).

Any diet will downregulate my energy expenditure, but who gives a fuck it will be back up after week og maintaince

This is variably false. Tripping up insulin chronically is the most optimal way to trash basal metabolic rate, or resting energy expenditure(REE). If you're doing CICO for extended periods of time the body also reduces BMR in response to match your energy in, a conservation of energy effect when ever you dip below caloric maintenance for any extended period of time.

Its known in people who do this acutely, such as the "Biggest Loser" contestants, their BMR is low despite the show concluding seven years prior. This was also discovered in war time with the Minnesota Starvation Experiment. Humans are quite well adapted to combating famine based responses. However people who do this slowly won't incur this physiological wrath for possibly months. Its still poorly understood because there's not enough research literature on the topic. But that's what it points to so far.

And yes it is just energy in energy out. It once again shows that you don't get this stuff, the energy balance cant be anything else because of physical laws

It is not even close to Newtonian, because the body isn't a linear energy system. If it was, all those periods of famine in the past would've massacred our ancestors outright. The body can and does mediate on "energy out" in response to "energy in" and will tap down on its Basal Metabolic Rate in order to effect a conservation of energy. One of the mechanisms for that is "Thermogenesis". Its also suspected it drains on power going to the brain and other systems, such as the immune system, etc to also effect this lowered BMR.

This is why CICO is an optimal yo-yo diet. Your personal experience is also severely confounded because most of the population doesn't go to the gym. What do you think mediates their weight? Diet, sleep, stress. Eating sugar, chronically will put the general population into a state of fat storing. Its also baked into the government recommendations for "The Standard American Diet".

To someone who's empirical the current disgraceful state of the US isn't a surprise. Its the result of macro economic policies that work towards incentivizing this effect on a general population.

There is also a reason why we use approximations, because they are good enough and the real process is to hard/not efficient to describe.

False again, its because there's no way to ascribe 100% certainly, especially when the physiology of people, the context of which is different for everyone. Most also think the labs are these infallible measure when they're not.

[–]Sumsar01-1 points0 points1 point 6 years ago (2 children) | Copy Link

Look man your on internet science wowo train. I don't really care to discuss keto tbh and feel free to use your time reading papers about it, but know that it's fucking boring, you have to read all the article not just the abstract and you need to read all/most of the litteratur before it's worth anything and as long as your protein (it's to low if you actually eat a keto diet) is the same your probably not going to see any benefits from keto unless you have diabetes. Your statement about fat burning simply isnt true. Yes keto have shown results in endurance athletes, but not in strength sport and your brain need glycogen. Bodybuildere, boxers, powerlifters etc. have lost weight for ages without downregulating REE im not really sure i care to much about weightloss literatur untill recently sustained weightloss wasnt even possible according to it. I don't really give a shit about merican diet or corporations or w/e my food is local. First of all im not some ape. Who the fuck use Newtonian mechanics. Second it doesnt fucking matter in any practical sense your body is linear in energy output if you have ever actually made a weight cut you would know that. If not good luck changing calorie consumption every single day based on special events in your body.

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Probably believe science that doesn’t hinge on creating or sustaining entire industries. Certainly there’s no bias when trillions of dollars are at stake.

Read:

climate “science”
nutrition “science”

Climate “science” is about total economic control of nations. Creating a “stock market” where globalists can control who has access to “carbon credits” (manufacture and production) as the god-king, saviors of mankind.

Nutrition science has already shown xenoestrogen to be extremely toxic, as evidenced by the rise of soy boy antifags and trannies and gays. Now do you think the gov has an interest in shutting down billions of dollars of gov subsidized soy agribusiness that produces weak, docile, and effeminate men that pose no threat to the globohomo orthodoxy? Of course not.

Of course soy is “safe”. Soy makes too much money and produces the desired results.

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Soy is an isoflavone, it has genistein in it. It disables the enzymatic precursors for testosterone. Soy isn't the only plant food with isoflavoniods, grains also have it too.

Other sources are kidney, navy, pinto, red, small white, and mung beans and chickpeas, split peas, peanuts, sunflower seed, and walnut. Raw soybeans can contain 1.2–4.2 mg g−1 dry weight isoflavones, while high-protein soy flour may contain up to 1.1–1.4 mg g−1 dry weight.

Safety concerns with soy are not new whatsoever but were directly ignored by special interests in the government.

Edit: there was a letter by two FDA employees around the time of soy's approval, I'll try to dig it up and repost it here.

Edit 2: SCIENTISTS PROTEST SOY APPROVAL

Scientists Protest Soy Approval

Researchers Daniel Doerge and Daniel Sheehan, two of the Food and Drug Administration’s experts on soy, signed a letter of protest, which points to studies that show a link between soy and health problems in certain animals. The two say they tried in vain to stop the FDA approval of soy because it could be misinterpreted as a broader general endorsement beyond benefits for the heart. The text of the letter follows.

To whom it may concern,

We are writing in reference to Docket # 98P-0683; “Food Labeling: Health Claims; Soy Protein and Coronary Heart Disease.” We oppose this health claim because there is abundant evidence that some of the isoflavones found in soy, including genistein and equol, a metabolize of daidzen, demonstrate toxicity in estrogen sensitive tissues and in the thyroid.

This is true for a number of species, including humans. Additionally, the adverse effects in humans occur in several tissues and, apparently, by several distinct mechanisms.

Genistein is clearly estrogenic; it possesses the chemical structural features necessary for estrogenic activity (; Sheehan and Medlock, 1995; Tong, et al, 1997; Miksicek, 1998) and induces estrogenic responses in developing and adult animals and in adult humans.

In rodents, equol is estrogenic and acts as an estrogenic endocrine disruptor during development (Medlock, et al, 1995a,b). Faber and Hughes (1993) showed alterations in LH regulation following developmental treatment with genistein.

Thus, during pregnancy in humans, isoflavones per se could be a risk factor for abnormal brain and reproductive tract development. Furthermore, pregnant Rhesus monkeys fed genistein had serum estradiol levels 50- 100 percent higher than the controls in three different areas of the maternal circulation (Harrison, et al, 1998). Given that the Rhesus monkey is the best experimental model for humans, and that a women’s own estrogens are a very significant risk factor for breast cancer, it is unreasonable to approve the health claim until complete safety studies of soy protein are conducted. Of equally grave concern is the finding that the fetuses of genistein fed monkeys had a 70 percent higher serum estradiol level than did the controls (Harrison, et al, 1998). Development is recognized as the most sensitive life stage for estrogen toxicity because of the indisputable evidence of a very wide variety of frank malformations and serious functional deficits in experimental animals and humans.

In the human population, DES exposure stands as a prime example of adverse estrogenic effects during development. About 50 percent of the female offspring and a smaller fraction of male offspring displayed one or more malformations in the reproductive tract, as well as a lower prevalence (about 1 in a thousand) of malignancies. In adults, genistein could be a risk factor for a number of estrogen-associated diseases.

Even without the evidence of elevated serum estradiol levels in Rhesus fetuses, potency and dose differences between DES and the soy isoflavones do not provide any assurance that the soy protein isoflavones per se will be without adverse effects.

First, calculations, based on the literature, show that doses of soy protein isoflavones used in clinical trials which demonstrated estrogenic effects were as potent as low but active doses of DES in Rhesus monkeys (Sheehan, unpublished data).

Second, we have recently shown that estradiol shows no threshold in an extremely large dose-response experiment (Sheehan, et al, 1999), and we subsequently have found 31 dose-response curves for hormone-mimicking chemicals that also fail to show a threshold (Sheehan, 1998a).

Our conclusions are that no dose is without risk; the extent of risk is simply a function of dose. These two features support and extend the conclusion that it is inappropriate to allow health claims for soy protein isolate.

[Continued in the link]

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Title	The 5 Ss of Xenoestrogen Warfare
Author	LastRevision
Upvotes	70
Comments	71
Date	August 20, 2019 11:42 PM UTC (6 years ago)
Subreddit	Posted in /r/TheRedPill
Original Link	https://old.reddit.com/r/TheRedPill/comments/ct8eh1/the_5_ss_of_xenoestrogen_warfare/
Archive Link	https://theredarchive.com/r/TheRedPill/the-5-ss-of-xenoestrogen-warfare.249833 https://theredarchive.com/post/249833

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