reSee.it - Tweets Saved By @holmanm

@holmanm - Marion Holman

1/13 When you've finished reading this I hope you realise how utterly insane the whole cholesterol lowering game is, and that the pharma industry is having a laugh at your expense. You are summoned to see your doctor. The conversation goes something like this. /2

@holmanm - Marion Holman

2/13 “Mr Jones, I’ve looked at your lipid profile and your Total Cholesterol number is just a tad above what it should be, and your good cholesterol is low 🤔 while your LDL is too high. We don’t need to worry about getting your LDL into single figures because it only kicks /3

@holmanm - Marion Holman

3/13 around as a modulator of innate and adaptive immunity and has some kind of job in repairing endothelial damage, so we can dispense with that nasty stuff. Now I have to say I’m obliged (according to our clinical guidelines) to prescribe a drug to lower your cholesterol. /4

@holmanm - Marion Holman

4/13 From what I can gather Lipitor is toxic at the 80mg and 40mg dosages, apparently contains Ochratoxin A and Citrinin at levels above human safety standards, but no worries, we’ll start you on the lower dose and hope you won’t experience too many serious side effects. /5

@holmanm - Marion Holman

5/13 If you do, we can always start on another Statin, or tweak the dose. The thing is Mr Jones, these drugs HAVE to be TOXIC because the way they work is the lactone portion of the mycotoxins contained in the drug is the active centre & binds to the HMG binding site of the /6

@holmanm - Marion Holman

6/13 Reductase molecule. I know it sounds rather complicated, but that’s the way in which the drug deprives all your cells of Mevalonate. Which by the way is a VITAL biochemical necessary for cell replication and stable cell membranes. To lower cholesterol you’ll have to /7

@holmanm - Marion Holman

7/13 accept that by blocking the Mevalanate pathway and up regulating your LDL receptors you are going to have to sacrifice a lot of cells. Well actually, those cells will undergo apoptosis ahem, (cell death). You may well ask why ? /8

@holmanm - Marion Holman

8/13 It’s because your cells are screaming out for Mevalonate and all those cells get is an overdose of cholesterol, which incidentally is toxic to cells. When enough cells have succumbed to the Mevalonate blockade you may find you experience a few issues such as brain fog, /9

@holmanm - Marion Holman

9/13 muscle pain, your blood glucose will definitely rise, and your CAC score may increase. Erm - what else ? Hmm Oh yes, heart failure, because Statins deprive cells of CoQ10. Have I forgotten anything ? Well, worst case scenario you may suffer some serious autoimmune /10

@holmanm - Marion Holman

10/13 condition such as Parkinson’s or ALS, or Rheumatoid Arthritis, but what the hell it's a small price to pay for getting those numbers a bit lower isn't it Mr Jones ? It may even reduce your health insurance premium if you get those numbers lower😂. /11

@holmanm - Marion Holman

11/13 Oh & by the way Mr Jones, the fact that your numbers are lower doesn’t mean you are actually lowering your risk of suffering a heart attack. It just looks really impressive on paper. In fact it’s highly likely that with lower cholesterol your risk of CVD is increased, /12

@holmanm - Marion Holman

12/13 but you know Mr Jones, guidelines, guidelines ……Come to think of it, Mr Jones the drug works in precisely the opposite way for which it was intended 🤔 but who am I question this ?. Computer says prescribe. Please let me know if you have any unpleasant “side effects” /13

@holmanm - Marion Holman

13/13 Mr Jones because we do have other drugs for those pesky little problems. Good luck Mr Jones, something tells me you might need it.😂" You think this reads like a comedy sketch ? The sad irony is that this happens each time YOU play Russian Roulette with your 'numbers'.

@holmanm - Marion Holman

13/13 Mr Jones because we do have other drugs for those pesky little problems. Good luck Mr Jones, something tells me you might need it.😂" You think this reads like a comedy sketch ? The sad irony is that this happens each time YOU play Russian Roulette with your 'numbers'.

@holmanm - Marion Holman

A prime example of Statin toxicity. Not all Statin "direct effects" are reversible, so please do the research and spare yourself this ⬇️⬇️

@holmanm - Marion Holman

1/5 Pharmacological evidence and clinical trial results support the interpretation that Statins stimulate atherogenesis by suppressing vitamin K2 synthesis and thereby enhancing artery calcification. Statins cause heart failure by depleting the myocardium of CoQ10, ‘heme A’ /2

@kasmha5150 - WhenPigsFly

@holmanm Where are the studies that show this information Marion? attach a link for us who want the details. Thanks.

@holmanm - Marion Holman

@kasmha5150 Who would pay for such studies ? Not the pharmaceutical industry, they would be shooting themselves in the foot. Get the truth by understanding the exact MOA of Statins. The books suggested will help, and of course any truly 'INDEPENDENT' research ⬇️ https://pubmed.ncbi.nlm.nih.gov/25655639/

Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms - PubMed In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the … pubmed.ncbi.nlm.nih.gov

@holmanm - Marion Holman

1/9 The presence of a Lp(a) in species that have lost the ability for endogenous vitamin C production has been one of the unsolved puzzles of science. Particularly compelling is the fact that the appearance of Lp(a) about 40 million years ago coincided with the loss of /2

@holmanm - Marion Holman

2/9 endogenous vitamin C synthesis by the ancestor of man. Based on this and other observations it has been proposed that Lp(a) functions as a substitute for vitamin C in stabilizing the Extracellular Matrix (ECM), particularly at times of prolonged nutritional scarcity. /3

@holmanm - Marion Holman

3/9 If this concept is confirmed, any pathological condition related to vitamin C deficiency would involve Lp(a) as compensating factor. In a previous study we confirmed this concept for cardiovascular disease, where a prolonged deficiency of dietary vitamin C leads to the /4

@holmanm - Marion Holman

4/9 deposition of Lp(a) in the vascular wall and the development of atherosclerotic plaques. Here we confirm this concept in cancer. In this condition, characterized by accelerated Extracellular Matrix Degradation (ECM) degradation and associated with vitamin C deficiency, /5

@holmanm - Marion Holman

5/9 Lp(a) contributes to PROTECT and RECONSTITUTE the ECM. In conclusion, our results indicate that the presence of Lp(a) in this animal model significantly decreased the development of primary tumors and metastatic tumors in the lung, suggesting that this molecule /6

@holmanm - Marion Holman

6/9 has anti-neoplastic properties. The histological detection of Lp(a) deposits in and around tumors suggest that this lipoprotein may participate in mitigating ECM damage during cancer progression, in particular by inhibiting proteolytic processes characteristic for /7

@holmanm - Marion Holman

7/9 all types of cancer cells. The results imply that due to its unique structure, Lp(a) may play a role in controlling tumor growth and expansion as a competitive inhibitor of plasmin-induced proteolysis and through its adhesive properties to ECM components. /8

@holmanm - Marion Holman

8/9 This study further confirms the concept that Lp(a) functions as a surrogate for ascorbate in disease and, thereby, stresses the role of ascorbate in fighting cancer. Patients clinically diagnosed with FH generally have elevated levels of Lp(a) 😉 https://www.spandidos-publications.com/10.3892/ijo.2016.3597#

Lipoprotein(a) and vitamin C impair development of breast cancer tumors in Lp(a)+; Gulo-/- mice Cancer progression is characterized by loss of extracellular matrix (ECM) integrity, which is a precondition for tumor growth and metastasis. In order to elucidate the precise mechanisms of ECM degradation in cancer we used a genetically modified mouse mimicking two distinct human metabolic features associated with carcinogenesis, the lack of endogenous vitamin C synthesis and the production of human Lp(a). Female Lp(a)+; Gulo(-/-) and control wild-type Balb/c mice without these two metabolic features were orthotopically inoculated with 4T1 breast cancer cells (5x105). The transgenic and control mice were divided into 4 different dietary groups in respect to dietary vitamin C intake: i) low ascorbate intake for 6 weeks; ii) high ascorbate intake for 6 weeks; iii) low ascorbate intake for 3 weeks followed by high ascorbate for 3 weeks; iv) high ascorbate intake for 3 weeks followed by low ascorbate for 3 weeks. After 6 weeks, all wild-type mice developed tumors. In contrast, Lp(a)+; Gulo(-/-) mice developed one third less primary tumors (low ascorbate diet) or no primary tumors at all (high ascorbate diet). Significantly, tumors from Lp(a)+; Gulo(-/-) mice immunostained positively for Lp(a) and their size was inversely proportional to Lp(a) serum levels. The results implicate that Lp(a) may play a role in controlling tumor growth and expansion. The most likely mechanism is the competitive inhibition of plasmin-induced ECM degradation due to the homology of Lp(a) components to plasminogen. The confirmation of this pathomechanism could lead to a universal therapeutic target for the prevention and treatment of cancer. spandidos-publications.com

@holmanm - Marion Holman

9/9 Given that Lp(a) is under strong genetic control, should we be trying to reduce Lp(a) with Statins/PCSK9's or would it make more sense to focus on ensuring that we have sufficient intake of Vitamin C as an antioxidant ? I favour the latter !

@bethshirley77 - Elizabeth Shirley

@holmanm C is only molecule that can reduce BH3 back to BH4. BH4 is what keeps NOS coupled to make nitric oxide. Without sufficient C, BH3 oxidizes to BH2 & uncouples NOS. Uncoupled NOS is a superoxide generator, not NO producer. Optimal NO prevents atherosclerosis....