1/ Ancel Keys has a lot to answer for. Researchers for the past 50 yrs have been beavering away in labs, desperate to find enough proof to covert the “lipid hypothesis” into the “Lipid FACT”. They have failed miserably, but in doing so have expanded
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2/ our knowledge of the biochemistry & physiology of the molecule CHOLESTEROL. Many researchers jumped the gun, & have discovered a type of Lipoprotein called small, dense (or type B) LDL which MAY be a risk factor for heart disease. Now here is the problem.
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3/ This small dense (type B ) LDL-C is WORSENED by the very diet recommended by those promoting the “lipid hypothesis”, and those who have hailed it for decades as the best diet to PREVENT heart disease. We are talking about the LOW FAT, high CARBOHYDRATE diet.
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4/ As it turns out, FAT, especially SATURATED fat DECREASES the amount of these small dense LDL particles, while the LOW FAT diet increases their number. The opposite of small dense LDL are large fluffy LDL particles, which are NOT harmful but are actually healthful.
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5/ Problem is that Statin drugs lower those too, & that's not all they do !!! Hmmm maybe we are on the wrong track here. When Cardios conclude that a therapeutic level of 100mg/dL for LDL is too 🔼 and needs to be even 🔽, we need to question their Lipochondriac herd mentality
**Convert** the lipid hypothesis !!
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1/ I laugh when studies talk about “unexpected results”.
These men were split into 2 groups
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Group (a) the intervention group, visited the investigators every 4th month. They were treated with intensive dietetic-hygienic measures & frequently with cholesterol lowering
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2/ drugs and blood pressure lowering drugs.
Group (b) the control group, were NOT treated by the investigators.
After 15 years, the study revealed: Wait for it !!!
- There was a 45% increase in deaths in the INTERVENTION group compared to the CONTROL group.
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3/ - There was a 142% increase in heart disease deaths in the INTERVENTION group compared to control
The results from this trial show that men who followed the Cholesterol lowering regime were MORE likely to die earlier and more than twice as likely to die of heart disease.
1/4 Today, researchers consider Atherosclerosis an inflammatory condition (similar to many other degenerative diseases whose cause is identified as chronic inflammation), rather than a lipid/high cholesterol problem. Some immunologists are even categorising Atherosclerosis as
2/4 a benign tumour. Hardening and narrowing of the arterial wall is a cumulative result of microscopic trauma, or infection. Inflammation occurs in the presence of OXIDISED lipids. Serrapeptase does NOT interfere with the synthesis of Cholesterol (Thank Goodness),
3/4 but acts as an anti-inflammatory and helps clear Avital tissue from the Arterial wall. Not only this but Serrapeptase significantly reduces hsCRP a primary marker for inflammation, and helps PREVENT LIPID OXIDATION. Serrapeptase is also anti-biofilm, so deals
1/7 The Fourier trial (Repatha) PCSK9 which lowers LDL cholesterol by 60%+ was ended early. It would have been embarrassing to see that the PLACEBO group had a LOWER mortality than the Repatha group ! However, that is exactly what happened.
2/7 Finally, the rate of all-cause mortality had started to diverge in favour of PLACEBO after 2 years of follow-up. It was 4.8% for Repatha and 4.3% for Placebo in participants with > 2.5 years of follow-up. A long-term follow-up would have yielded more events and thus more
3/7 power to evaluate the effect of Repatha on all-cause mortality. However, let’s bury the truth, by halting the trial early
1/4 Spoke to my friend who serves in my local shop today. She HAD trigger finger for several months. Was wearing a wrist & finger brace, and in a lot of pain. The only solution from her Doctor's point of view was to initiate Steroid
2/4 injections into the finger & prescribe NSAID's. I told her about Serrapeptase, and gave her a few of mine. She ordered some on the web and continued with Serrapeptase. She went to her GP yesterday and told him her trigger finger had completely resolved. Doc said
3/4 "Oh I'm so pleased that the Steroids have lasted much longer this time. Her reply "It's not the Steroids, it's the Serrapeptase ! Steroids were VERY short acting and painful. He wasn't in the least bit interested in Serrapeptase, but this girl rocks.
1/9 The Nobel Prize in Physiology or Medicine 1985 was awarded jointly to Michael S. Brown and Joseph L. Goldstein "for their discoveries concerning the regulation of cholesterol metabolism." What they should have been given is a very long prison sentence for killing a vast
2/9 swathe of the world population via Statin drugs.
Brown said in his Nobel speech that “Statins trigger a complex regulatory mechanism that sets a new steady state in cells.” He was perfectly correct. Statins neutralise reductase then increase reductase and LDL Receptors.
3/9 This SHIFTS LDL cholesterol from the serum to the LDL receptors on cells. This satisfies cells’ demand for Cholesterol but NOT ISOPRENOIDS, and sets a new homeostasis for REDUCTASE - Less elevated than at first, but nevertheless still elevated above normal.
1/7 Mycotoxins are fungal metabolites with pharmacological activities that have been utilized in the production of Statins, antibiotics, growth promoters, and other classes of drugs. Some mycotoxins have been developed as biological and chemical warfare agents.
2/7 Bombs and ballistic missiles loaded with aflatoxin were stockpiled and may have been deployed by Iraq during the first Gulf War. In light of the excess incidence of amyotrophic lateral sclerosis (ALS) in veterans from Operation Desert Storm, the potential for delayed
3/7 neurotoxic effects of low doses of mycotoxins should be a wake up call. I’ve lost count of the amount of new cases of ALS/MND, Parkinson’s, & other autoimmune diseases for those taking Statins. Next time you get your prescription filled for 80mg or 40mg of Lipitor, ask your