Posts made by haidut

Two of the features of aging thought to be unavoidable are brittle bones and increased visceral fat, both of which (alone or in combination) are a major contributing factor for the increased mortality seen with aging. As it turns out, both these features are apparently driven by decline in metabolism/OXPHOS, which is driven primarily by a relative NAD+ deficiency (i.e. low NAD+/NADH ratio), and supplementation with NAD+ precursors such as niacinamide may be able to stop/reverse them.

https://www.xiahepublishing.com/2835-6357/FIM-2023-00046

https://www.eurekalert.org/news-releases/1054674

“…Recent studies indicate that oxidative phosphorylation plays a critical role in osteogenesis, the process by which new bone is formed. During osteogenic induction, cells shift their energy metabolism from glycolysis to mitochondrial oxidative phosphorylation, increasing respiratory enzymes, mitochondrial DNA copy number, oxygen consumption, and intracellular ATP content​. Bone morphogenetic protein 2 (BMP2) has been shown to trigger metabolic adaptations in mesenchymal stem cells (MSCs), characterized by successive activation of glycolysis and oxidative phosphorylation​. NAD+ levels and the NAD+/NADH ratio are crucial for mitochondrial function, linking cellular metabolism to transcriptional events and signaling pathways. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, promotes osteogenesis and reduces adipogenesis in MSCs, protecting bone from aging and damage.”

Via: http://haidut.me/?p=2604

A very interesting study, which suggests niacinamide may be a treatment for depression. Strikingly, the almost 50% reduction in depressive symptoms occurred after just 4 weeks of consuming vinegar – a feat that almost no pharma antidepressant drug can currently match. I just hope the takeway from the blog post -is to use niacinamide for depression, instead of vinegar, since high levels of acetic acid promote fat synthesis and tumor growth and as such chronically elevated vinegar intake is probably not safe. The mechanism of action is mostly likely linked to the role of niacinamide as an NAD+ precursor, resulting in improved metabolism/OXPHOS. Of course, that strongly suggests (yet again) that depression is a metabolic disease:-)

https://www.mdpi.com/2072-6643/16/14/2305

https://www.phillyvoice.com/vinegar-depression-mood-mental-health/

“…A few tablespoons of vinegar a day may help keep depression away, research shows. Consuming two tablespoons of red wine vinegar twice a day for four weeks significantly improved self-reported depression scores in a group of 28 overweight adults who were otherwise healthy, a new study found. Enhancements in niacin metabolism may contribute to the improvement in mood, the researchers concluded.”

“…Vinegar, a combination of acetic acid and water made through fermentation, previously has been linked to positive outcomes for heart disease and weight loss. For the latest study, published in the journal Nutrients, researchers from the University of Arizona looked at how daily vinegar consumption affected mood and metabolism. They compared one group of people who took diluted vinegar daily to a second group that ingested a pill containing very little vinegar. By the fourth week, the group taking the diluted vinegar showed a 42% reduction in depression scores compared to an 18% reduction in the group taking pills. The group that drank the vinegar daily also experienced an 86% increase in levels of nicotinamide, a form of vitamin B that has been linked to anti-inflammatory effects.”

Via: http://haidut.me/?p=2602

Chronic obstructive pulmonary disease (COPD) rates have been steadily rising over the last 2-3 decades despite steadily decreasing rates of smoking in the general population. COPD rates have further increased after the COVID-19 pandemic, and drastically increase all-cause mortality not only from lung failure buy from cardiovascular disease (CVD), diabetes, cancer, etc. As such new treatments are urgently needed. The study below demonstrates that higher vitamin E intake may protect from the increased all-cause mortality seen in COPD patients. While the proposed mechanism of action is, again, the known antioxidant effects of vitamin E the real mechanism of action probably has more to do with the ability of vitamin E to decrease the synthesis of the highly inflammatory PUFA metabolites known as prostaglandins and leukotrienes. The anti-estrogenic effects of vitamin E probably also play a role, as estrogen is known to exacerbate COPD and some studies have even demonstrates a causative effects of COPD by estrogen de-novo. The effect was dose-dependent, which suggests doses higher than the puny RDA would be needed for optimal effects. While the study did not state this directly, the authors discuss the protective effects of other anti-oxidants such as vitamin C in respiratory conditions such as COVID-19, which suggests that vitamin E may be protective in COVID-19 as well, which has already been confirmed by human studies.

https://www.dovepress.com/higher-vitamin-e-intake-reduces-risk-of-all-cause-mortality-and-chroni-peer-reviewed-fulltext-article-COPD

“…For this study, we utilized the NHANES database, which is rich in content, scientific, and reliable. Previous studies have found that VE intake is positively associated with lung function25 and negatively associated with the risk of COPD.23 Our study confirmed that dietary VE intake was also inversely associated with all-cause and CLRD deaths in COPD, with a significant dose-response relationship through a generalized additive model. There was no significant correlation with CVD death in COPD patients. COPD is a leading cause of morbidity, mortality and healthcare consumption worldwide,29 which is caused by exposure to inhaled toxic particles, especially tobacco smoke and pollutants.30 In recent years, increasing attention has been paid to a wide range of factors that increase the risk of COPD development and progression throughout the life course, including early lung development and infection.1 Dietary factors might modulate the effects of adverse environmental exposures or genetic predisposition on the lungs, but may also have direct (protective or harmful) effects on biological processes involved in lung function, disease development and outcome.31–33 Vitamins are a group of organic compounds that are essential to the physiological functioning of the body. Vitamin content has a positive significance in the development of the lungs and already plays a role in the development of the foetal lungs during pregnancy.34,35 At the same time, vitamins, as the main dietary nutrients, are the regulatory factors of immune response, and their influence on human immunity is crucial.36 Pulmonary respiratory infection in childhood has an important influence on the trajectory of pulmonary function changes in adults and can increase the prevalence of COPD.37 Dietary interventions early in life may help lung function remain stable throughout life. What’s more, in a randomised trial, the role of vitamin C in preventing acute respiratory infections (ARI) was stronger in men and middle-income countries compared with adult women and high-income countries, respectively.38 During COVID-19, a controlled study confirmed that supplementation with 1 g/d vitamin C reduced symptoms and shortened disease duration, thereby improving recovery rates.39“

Via: http://haidut.me/?p=2600

Evil serotonin rears its ugly head again. This time, the findings of the study below are that serotonin may be the primary driver of post-surgical pain, which often becomes chronic and may lead to depression, opioid/alcohol addiction, anti-social behavior, etc. So much for serotonin being the “cure” of depression. Now, while the study below looked only at post-surgical pain, in my opinion the findings are not specific to that situation only. Namely, the inflammatory state (driven by mast cell activation), which most patients find themselves in after surgery is characterized by inflammatory mediators found systemically and not just in the organ/tissue operated on. This means that serotonin may be responsible for many/most cases of “idiopathic” chronic pain seen in people without physical trauma or surgery. Interestingly, systemic inflammation and chronic pain are a common observation in depression, which may explain why anti-inflammatory drugs (many of which are also analgesics) are often therapeutic in depression.  Furthermore, many studies have observed a very strong correlation between levels of inflammation and chronic pain and severity of depressive symptoms. As such, one can plausibly conclude that the administration of SSRI drugs directly promotes at the very least chronic inflammation and pain, and likely depression as well. Unfortunately, I suspect it will be decades before we see such a direct conclusion in a study like the one below, published in a highly reputable journal.

The study used genetic deletion of the enzyme tryptophan hydroxylase (TPH), which produced serotonin, in order to block the post-surgical pain. This method is obviously not practical to implement in humans, so instead one could probably achieve the same effects using serotonin antagonists such as cyproheptadine and metergoline, or the (even better) the over-the-counter anti-acid drug famotidine, which was found to be a powerful anti-serotonin agent capable of stopping already established serotonin syndrome (which is often lethal).

https://www.science.org/doi/10.1126/sciimmunol.adh0545

“…Inflammation caused by surgical tissue injury can evolve into chronic pain. Starkl et al. used a mouse model of surgical tissue injury to decipher a role for mast cell–derived metabolites in postoperative pain. Tetrahydrobiopterin (BH4) has been previously detected in injured nerves and correlates with pain intensity and is required for serotonin production by tryptophan hydroxylase (Tph1). Nerve-proximal mast cells were identified as a source of GTP cyclohydrolase 1 (Gch1), a rate-limiting enzyme for BH4 synthesis. Deletion of Gch1 or Tph1 from mast cells or mast cell depletion reduced tissue injury pain. The nociceptive neuropeptide substance P was detected at tissue injury sites and triggered BH4-dependent serotonin release from mast cells, thus defining how neuropeptides can act on mast cells and propagate pain responses.”

“…Postoperative pain affects most patients after major surgery and can transition to chronic pain. The considerable side effects and limited efficacy of current treatments underline the need for new therapeutic options. We observed increased amounts of the metabolites BH4 and serotonin after skin injury. Mast cells were primary postoperative sources of Gch1, the rate-limiting enzyme in BH4 synthesis, itself an obligate cofactor in serotonin production by tryptophan hydroxylase (Tph1). Mice deficient in mast cells or in mast cell–specific Gch1 or Tph1 showed drastically decreased postoperative pain. We found that injury induced the nociceptive neuropeptide substance P, mast cell degranulation, and granule nerve colocalization. Substance P triggered serotonin release in mouse and human mast cells, and substance P receptor blockade substantially ameliorated pain hypersensitivity. Our findings highlight the importance of mast cells at the neuroimmune interface and substance P–driven mast cell BH4 and serotonin production as a therapeutic target for postoperative pain treatment.”

Via: http://haidut.me/?p=2598

Ever since we launched our B-complex product Energin almost 10 years ago, we have been getting emails about why the product does not contain folic acid and vitamin B12. I keep answering by saying that both of those vitamins have been linked to higher risk of cancer, and as such have stubbornly resisted demands to add those 2 vitamins to the product. Now, the study below adds another good reason to not take folate supplement in adulthood – reduced folate intake may increase lifespan. Interestingly, the mechanism of action for lifespan extension by folate restriction is that dietary folate deficiency seems to restore metabolic flexibility – a hallmark of youth. While we easily switch between burning carbs and fat in our childhood and early adulthood, that flexibility declines as we age. Very old (or sick) people burn predominantly fat, even in the presence of sufficient glucose intake. This lack of metabolic flexibility is likely driven by a steady decline in thyroid function as we age, which results in compensatory increase in adrenal activity, with the end result being that older people are in a state of chronic stress even when undisturbed, which results in excessive lipolysis and thus dominance of fat oxidation as per the Randle Cycle. Whether restricting dietary folate results in increased thyroid function, reduced adrenal hyperactivity, or both remains to be discovered. Be that as it may, the main (indirect) finding of the study seems to be that lifespan is metabolically controlled, and restoring youthful metabolic profile can extend lifespan.

https://pubmed.ncbi.nlm.nih.gov/38260683/

“…Folate is a vitamin required for cell growth and is present in fortified foods in the form of folic acid to prevent congenital abnormalities. The impact of low folate status on life-long health is poorly understood. We found that limiting folate levels with the folate antagonist methotrexate increased the lifespan of yeast and worms. We then restricted folate intake in aged mice and measured various health metrics, metabolites, and gene expression signatures. Limiting folate intake decreased anabolic biosynthetic processes in mice and enhanced metabolic plasticity. Despite reduced serum folate levels in mice with limited folic acid intake, these animals maintained their weight and adiposity late in life, and we did not observe adverse health outcomes. These results argue that the effectiveness of folate dietary interventions may vary depending on an individual’s age and sex. A higher folate intake is advantageous during the early stages of life to support cell divisions needed for proper development. However, a lower folate intake later in life may result in healthier aging.”

https://www.medicalnewstoday.com/articles/could-eating-less-folate-vitamin-b9-actually-help-aging-metabolisms#Why-folates-are-important-for-health

“…A new study suggests that while consuming folates is considered healthy for everyone — and it clearly benefits the young — it may result in metabolic issues for older individuals. The study of mice from Texas A&M University’s AgriLife Research found that lower levels of folates, the naturally occurring form of vitamin B9, facilitated the transition from sleep metabolism to waking metabolism…The study’s senior author, Michael Polymenis, PharmD, PhD, who teaches biochemistry and biophysics at Texas A&M, told Medical News Today, “As we age, we cannot switch quickly from one mode of metabolism (e.g., burning fat while we sleep) to another (e.g., burning carbs when we wake up). Quick transitions are necessary to meet our body’s on-demand needs.” Michelle Routhenstein, MS, RD, CDCES, preventive cardiology dietitian at EntirelyNourished.com, who was not involved in the study, explained, “During the day when active, the body primarily uses carbohydrates for energy, with higher insulin levels facilitating glucose uptake. At night, insulin sensitivity decreases, shifting metabolism toward using stored fat, as the body’s energy needs are lower, and growth hormone levels increase.” “As we age,” said Polymenis, “our bodies become less adept at adjusting their fuel source in response to changing needs, which can affect overall health and energy levels.”

Via: http://haidut.me/?p=2596

Over the last 5-6 years, a number of high profile articles (many of them, including the new one below, published in the top journal Nature) confirmed lactate as not only an “oncometabolite”, but as a direct driver of cancer growth, aggressiveness, metastases, and ultimately death of the patient. Lactic acidosis type B, which is often seen in patients with advanced cancer, has about 40% lethality even if the patient is in the hospital and receiving the most advanced treatments available for metabolic acidosis. So, nothing benign or insignificant about lactate, as medicine would have us believe. The new study below now demonstrates that lactate has another “trick” up its sleeve – i.e. increasing resistance of the “cancer” cells to chemotherapy. I shudder at the thought of how many cancer (and other) patients deteriorate (or even die) iatrogenically due to the administration of the so-called “Ringer Lactate” solution – a common “hydration” therapy given by IV in hospitals to critically ill patients, including cancer patients. But I digress.

Interestingly, lactate achieves this enhanced resistance to chemotherapy by increasing the activity of enzymes involved in DNA repair inside “cancer” cells. Since such cells are known to have a high rate of DNA damage/mutation, it makes sense that “cancer” cells have increased DNA repair processes. However, most of the DNA repair processes consume a lot of NAD+, especially the PARP-1 and CD38 enzymes, which further lowers the critically-important mitochondrial NAD+/NADH ratio in the already highly reductive “cancer” cells. Conversely, PARP-1 and CD38 inhibitors have been shown to be therapeutic for cancer, which is undoubtedly due to the ability of such inhibitors to “spare” the NAD+ the sick organism so desperately needs. Thus, the main mechanism of lactate’s pro-cancer effects may very well turn out to be its NAD+ depletion by activating DNA repair in “cancer” cells. To make matters worse, lactate is itself a reductant and consumes NAD+ directly when it is oxidized back to pyruvate by the enzyme lactate dehydrogenase (LDH). Interestingly, the study found that inhibition of lactate generation by the administration of an LDH inhibitor was therapeutic and cancelled the resistance of “cancer” cells to chemotherapy. Now, if only there was a way to attack all of those pathways simultaneously with a simple, cheap and safe molecule…Luckily, niacinamide is just such a substance. Not only is niacinamide the main endogenous precursor to NAD+, but it is also a powerful inhibitor of the NAD+ consuming enzymes PARP-1 and CD38. Thus, niacinamide raises NAD+ by being both a precursor and inhibitor of NAD+ consumption. In corroboration, niacinamide has been shown to reliably lower lactate in humans. Other powerful lactate generation inhibitors include vitamin B1 (thiamine) and vitamin B7 (biotin). Coincidentally, the combination of those vitamins, together with aspirin, was able to induce complete regression in my recent xenograft study with the human jeko-1 (mantle cell lymphoma) cell line. Thus, we can conclude once again that “cancer” is metabolic in origin and likely just a symptom of a highly reduced (both literally and figuratively) metabolic state, and administering substances that shift the metabolic state towards oxidation may very well cure the “cancer”. Oh, and last but not least, the study discloses (perhaps inadvertently) that LDH inhibitors are used clinically for the treatment of epilepsy – a condition medicine considers both mysterious in origin and incurable. Thus, I think we can safely conclude that epilepsy, just like cancer, is also nothing but a symptom of severe (brain) energetic depletion, and also amenable to simple treatment as described above:-)

https://www.nature.com/articles/d41586-024-02731-9

“…The molecule lactate is a waste product of the metabolism of sugar without oxygen — a metabolic pathway preferentially used by cancer cells to generate their energy. Metabolomics analysis reveals that lactate in tumour cells promotes resistance to chemotherapy, and sheds light on the molecular mechanism that underlies this unexpected role of lactate in cancer.”

https://www.nature.com/articles/s41586-024-07620-9

“…The Warburg effect is a hallmark of cancer that refers to the preference of cancer cells to metabolize glucose anaerobically rather than aerobically1,2. This results in substantial accumulation of lacate, the end product of anaerobic glycolysis, in cancer cells3. However, how cancer metabolism affects chemotherapy response and DNA repair in general remains incompletely understood. Here we report that lactate-driven lactylation of NBS1 promotes homologous recombination (HR)-mediated DNA repair. Lactylation of NBS1 at lysine 388 (K388) is essential for MRE11–RAD50–NBS1 (MRN) complex formation and the accumulation of HR repair proteins at the sites of DNA double-strand breaks. Furthermore, we identify TIP60 as the NBS1 lysine lactyltransferase and the ‘writer’ of NBS1 K388 lactylation, and HDAC3 as the NBS1 de-lactylase. High levels of NBS1 K388 lactylation predict poor patient outcome of neoadjuvant chemotherapy, and lactate reduction using either genetic depletion of lactate dehydrogenase A (LDHA) or stiripentol, a lactate dehydrogenase A inhibitor used clinically for anti-epileptic treatment, inhibited NBS1 K388 lactylation, decreased DNA repair efficacy and overcame resistance to chemotherapy. In summary, our work identifies NBS1 lactylation as a critical mechanism for genome stability that contributes to chemotherapy resistance and identifies inhibition of lactate production as a promising therapeutic cancer strategy.”

Via: http://haidut.me/?p=2594

The study was with humans, which makes it that much more relevant. As most of my readers know, sleep deprivation is a definitely a “thing” in most Western countries, and it has serious health consequences such as increasing risks of infertility, diabetes, dementia, heart disease, cancer, etc. The response by Big Pharma has been to release a number of different sleeping pills (Ambien, anyone?) the vast majority of which have terrible side effects, and most importantly do not resolve neither the underlying reason for the insomnia, nor its inflammatory effects. The study below demonstrates that humble aspirin may be able to achieve what billions of dollars wasted by Big Pharma on sleeping pills R&D cold not. Namely, prevent/resolve the brain inflammation driven by chronic sleep deprivation, as well as ameliorate the cognitive dysfunction driven by said brain inflammation. It is worth pointing out that for the in-vitro portion of the study, the scientists used endotoxin/LPS to cause the brain cell inflammation. Chronic, low-grade endotoxemia is definitely also a “thing” in most modern societies and apparently aspirin can help with that as well.

https://article.imrpress.com/journal/FBL/26/6/10.52586/4928/Landmark4928.pdf

https://www.news-medical.net/news/20240603/Low-dose-aspirin-can-reduce-inflammatory-responses-to-sleep-restriction.aspx

Aspirin Eases Inflammation from Sleep Loss

“…Results show that compared with placebo, preemptive administration of low-dose aspirin during sleep restriction reduced pro-inflammatory responses. Specifically, aspirin reduced interleukin-6 expression and COX-1/COX-2 double positive cells in lipopolysaccharide-stimulated monocytes, as well as C-reactive protein serum levels.”

“…“The novelty of this study is that it investigated whether we can pharmacologically reduce the inflammatory consequences of sleep restriction,” said lead author Larissa Engert, who has a doctorate in behavioral physiology and is a postdoctoral fellow in the department of neurology at Beth Israel Deaconess Medical Center and the division of sleep medicine at Harvard Medical School in Boston. “We used a non-steroidal, anti-inflammatory drug because it has been shown to affect specific inflammatory pathways, which were previously shown to be dysregulated by experimental sleep restriction or sleep disturbances.”

Via: http://haidut.me/?p=2592

Actual conclusion of the study itself and a very strong claim, considering medicine considered OA to be incurable and progressive. While the study claims that reduced inflammation is the main mechanism of action of vitamin B1 supplementation, I think the much more likely explanation is the simple fact that B1 is a crucial factor for the oxidative metabolism of glucose and the generation of CO2. In fact, vitamin B1 is often given clinically as a supplementat to lower lactate and raise CO2. While medicine considers CO2 as little more than “metabolic waste”, a well-known fact is that the deposition of calcium into the bones depends on the carboxylation (i.e. using CO2) of various bone building proteins such as osteocalcin. Thus, elevated CO2 levels directly result in denses, bigger, stronger bones while lower CO2 levels (which means higher lactate) result in bone resorption, and elevated serum calcium and excretion. Thus, in the context of elevating CO2 the effects of vitamin B1 make perfect sense, and in fact can be further increased by adding niacinamide and biotin, both of which have also been shown to lower lactate and raise CO2 levels. Btw, this CO2-raising, synergistic effect of B1, B3, and B7 (biotin) is one of the main reasons I chose those vitamins for the cancer studies I am currently running.

https://pubmed.ncbi.nlm.nih.gov/39024114/

“…As the primary cause for chronic pain and disability in elderly individuals, osteoarthritis (OA) is one of the fastest-growing diseases due to the aging world population. To date, the impact of microenvironmental changes on the pathogenesis of OA remains poorly understood, greatly hindering the development of effective therapeutic approaches against OA. In this study, we profiled the differential metabolites in the synovial fluid from OA patients and identified the downregulation of vitamin B1 (VB1) as a metabolic feature in the OA microenvironment. In a murine destabilization of medial meniscus-induced OA model, supplementation of VB1 significantly mitigated the symptoms of OA. Cytokine array analysis revealed that VB1 treatment remarkably reduced the production of a pro-OA factor-C-C Motif Chemokine Ligand 2 (CCL2), in macrophages. Further evidence demonstrated that exogenous CCL2 counteracted the anti-OA function of VB1. Hence, our study unveils a unique biological function of VB1 and provides promising clues for the diet-based treatment of OA.”

“…Additionally, Fursultiamine, a VB1 derivative, was found to improve the therapeutic effect of glucosamine hydrochloride plus chondroitin sulfate in OA (11). In this study, we systemically profiled the metabolic changes in the OA microenvironment and identified VB1 as one of the most dramatically changed metabolites. The anti-OA function of VB1 is at least partially attributed to its capacity to suppress CCL2 expression. Compared to other chemokines, CCL2 plays a particularly crucial role in OA progression. OA patients exhibited increased CCL2 production in the synovial fluid compared to healthy controls (12). Mechanistically, CCL2 may exacerbate OA by mediating the recruitment of peripheral monocytes (13), inducing the expression of MMPs and VCAM-1 (12, 14), increasing the activity of collagenase (15), or promoting cartilage damage (16) or facilitating the production of inflammatory cytokines (17). As a natural and water-soluble vitamin, VB1 has relatively higher safety and lower costs compared to traditional anti-OA drugs, potentially enhancing patient compliance. Thus, increasing the intake of VB1-rich food (such as whole grains, beans, nuts, and fish) is a potentially beneficial dietary approach in OA patients. Taken together, in this study, we identified a safe, natural nutrient (VB1) that prevents the pathological processes of OA, thereby providing unique perspectives on dietary interventions for OA.”

Via: http://haidut.me/?p=2590

Reduced frequency of bowel movements is one of the most reliable signs of declining metabolic rate, and it just happens to be one of the most common signs of aging. Reduced bowel movements are also the main factor behind chronic, low-grade endotoxemia seen in most adults over 35, and this endotoxemia is now recognized as a culprit behind virtually every chronic disease known to medicine. Conversely, constipation relief is one of the reliable indicators of increased metabolic rate and has been demonstrated to result in reduced inflammation, both in the GI tract and systemically. Medicine has already recognized chronic constipation as a reliable sign of impending ill health, but the “solutions” it offers are at best misguided and at worst may exacerbate the underlying metabolic problems. In other words, the laxatives sold OTC in most stores are probably something to be avoided. Even the relatively benign magnesium hydroxide can cause GI irritation when taken in doses that result in increased motility. The study below may have a simple solution – vitamin B1, also known as thiamine. Vitamin B1 is crucial for the oxidative metabolism of glucose and for the production of CO2. Increasing CO2 levels in the GI tract has already been shown to resolve constipation and possibly even serious conditions such as inflammatory bowel disease (IBD). The study below suggests taking some extra B1 may be a simple and cheap way of resolving constipation, and thus systemic and digestive inflammation.

https://bmcgastroenterol.biomedcentral.com/articles/10.1186/s12876-024-03255-2

https://www.medscape.com/viewarticle/vitamin-b1-may-help-lower-constipation-risk-adults-2024a1000dey?form=fpf

“…”This association suggests that enhanced intake of vitamin B1 through diet may facilitate softer stools and heightened intestinal motility, thereby potentially alleviating constipation symptoms. Consequently, healthcare professionals are advised to prioritize the promotion of a well-balanced diet as an initial therapeutic approach, preceding medical interventions,” the authors wrote.”

Via: http://haidut.me/?p=2588

An interesting study, considering vitamin E’s benefits are thought (by medicine) to be mostly related to its anti-oxidant effects, while the condition chronic obstructive pulmonary disease (COPD) is thought to be related mostly to external factors such as smoking, air pollution, respiratory infections, etc. Despite the study pushing the anti-oxidant angle, my opinion is that the preventive effects of vitamin E were mostly due to its role as COX and LOX inhibitor, which makes it a powerful anti-inflammatory substance, and COPD is at its core an inflammatory disorder. Now, since COX and LOX produce inflammatory mediators (prostaglandins and leukotrienes, respectively) from PUFA, the findings of the study suggest COPD is yet another PUFA-driven disorder. In addition, estrogen is known to exacerbate (or maybe even cause?) COPD and the anti-estrogenic effects of vitamin E probably also play a role in its preventive effects for this condition. The study did not look into therapeutic effects, but given the animal studies showing COPD alleviation/reversal by vitamin E (through its role as COX inhibitor), it would probably be not too far-fetched to say that vitamin E may also treat established COPD if taken in higher doses for sufficiently long time. Avoidance of PUFA will probably also have the same beneficial effects, on both prevention and treatment.

https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2023.1124648/full

Higher vitamin E intake linked to lower COPD risk: US data

“…Findings indicate that vitamin E supplementation may help in preventing COPD, but more research is needed to confirm this, researchers note. The study “Association of Dietary intake of vitamin E with chronic obstructive pulmonary disease events in US adults: A cross-sectional study of NHANES 2013-2018,” was published in Frontiers in Nutrition. ”

“…Results showed the highest intake group had a significantly reduced risk of COPD, by 43%, relative to the lowest intake group. Those on medium levels of vitamin E intake also tended to have a lower COPD risk than those on the lowest levels, but this difference wasn’t statistically significant, which means it’s mathematically plausible it could be random chance. Further statistical analyses, as well as subgroup analyses, all indicated the higher the vitamin E intake, the lower the risk of developing COPD. “The results showed that vitamin E intake among U.S. adults was well below the recommended levels and that higher vitamin E intake was negatively associated with COPD incidence,” the scientists wrote. Based on these findings, vitamin E supplementation might “have an important role in the prevention of COPD,” the team wrote.”

Via: http://haidut.me/?p=2586

Just a day ago I did a post about estrogens being a cause of dementia, while anti-estrogens being therapeutic. Now, the study below found that estrogen causes anxiety – the most common mental health condition worldwide. Considering estrogen, in the form of ethinyl estradiol, is in virtually all birth control pills, devices, patches, etc prescribed worldwide one would be forgiven for thinking that the most widespread mental health issue (anxiety) is nothing but a symptom of the mass-usage of estrogen, willingly and willingly. Why unwillingly? Well, even people who do not use hormonal birth control are exposed to a myriad of endocrine disruptors that are used in everything from food packaging, to store receipts, to household item production, to cosmetics, to drugs, etc. The vast majority of these endocrine disruptors are potent (xeno)estrogens, and many of them are much more potent than the endogenous estrogen estradiol. The good news is that simply increasing the metabolic rate seems to be sufficient to be able to get rid of those endocrine disruptors, though cessation of estrogen usage (as in birth control) is also something everybody knowingly using estrogen should probably seriously consider. The study opined that the reason for the anxiety was the decline in testosterone levels that estrogen administration caused. However, I suspect that the decline of progesterone levels (which estrogen also caused) is the more likely explanation since progesterone is the primary steroidal GABA agonist and reducing the levels if pro-GABA substances in the body is known to reliably cause anxiety. Testosterone is a weak-to-ineffective GABA agonist compared to progesterone.

https://www.medicalnewstoday.com/articles/synthetic-estrogen-birth-control-anxiety-rats#How-hormonal-contraceptives-affect-behavior

https://www.msn.com/en-us/health/other/hormonal-havoc-synthetic-estrogen-and-its-role-in-anxiety/ar-BB1oIyf0?item=flightsprg-tipsubsc-v1a/

“…A study shows that synthetic estrogen, the primary ingredient in oral contraceptives, can increase anxiety. The results of a murine study on the relationship between ethinylestradiol, a synthetic estrogen, and anxiety behavior were presented at the annual endocrinology conference ENDO 2024. ”

“…The study revealed that mice given ethinylestradiol struggled with the spatial memory task during the maze test, unlike other mice. This indicates a heightened level of anxiety in the mice. Furthermore, serum sample analysis showed a decrease in the levels of male hormone testosterone and progesterone. The researchers explained that a decrease in testosterone, which typically reduces anxiety behavior and improves spatial memory, may have been due to ethinylestradiol, leading to increased anxiety behavior. Based on these findings, the researchers concluded that synthetic estrogen ingredients can increase anxiety behavior in mice.”

Via: http://haidut.me/?p=2584

Well, it does not get any clearer than the findings of the study below. Namely, the old saying is true – we don’t see things the way they are, we see things the way we are. More specifically, the  study claims that the positivity/negativity of our life experience and outlook on the world depend mostly on energy production in the brain, with the effects being bidirectional. Apparently, brain energy production is extremely sensitive to the functioning of electron transport chain (ETC) Complex I, which oxidizes NADH back into NAD+. That process depends on the availability of FAD/FMN and Coenzyme Q10 (CoQ10), and is easily inhibited by a variety of physical, chemical and social factors. One of the most widely prescribed drugs worldwide – metformin – is a powerful inhibitor of Complex I. Chronic stress (even mild in intensity) not only inhibits Complex I, but also reduces its expression, thus causing structural deficits in the machinery that produces energy. The resulting reductions in energy production in the brain result in negative psychosocial experiences, which are perceived as stress by the brain, which leads to further decline in energy production, and so on. In other words, a perfect vicious cycle. The opposite also seems to be true. Good experiences increase energy production in the brain, resulting in positive world perceptions, leading to further increase in energy production, and so on. The study cites numerous other experiments demonstrating that many mental health issues (anxiety, depression, psychosis, mania, etc) can be reliably caused in animals by interfering with energy production in the brain. Thus, the epidemic of mental illness seen in Western countries is likely nothing more than a symptom of the chronic stress people in those countries are experiencing, despite the claims of their governments that everything is great and things are betting better by the day. Aside from trying to improve out lifestyle and reduce stress, which is very difficult to achieve for most people living a “modern” lifestyle,  another option would be to supplement with things that support brain energy production and especially Complex I. Such substances include vitamin B2 (precursor to FAD/FMN), CoQ10 (the oxidized version – uniquinone – not ubiquinol), niacinamide (precursor to NAD+), aspirin, thyroid, etc.

https://pubmed.ncbi.nlm.nih.gov/38889126/

Study Links Stress to Mitochondrial Dysfunction in the Brain

“…For the first time, scientists have shown that the abundance of proteins needed for mitochondrial energy production in human brains is linked to perceived psychosocial experiences [1]. ”

“…One such factor, OxPhos protein abundance, relates to the amount of protein available for oxidation-phosphorylation reactions, which are at the core of mitochondrial energy production. In the dorsolateral prefrontal cortex (DLPFC), a brain area that is involved in executive functions and emotional regulation and is known to be sensitive to psychological stress, this factor showed marked correlation with both positive and negative psychosocial experiences. The positive psychosocial aspects most associated with increased OxPhos protein abundance were well-being and late-life social activity. On the opposite side of the scale, negative mood and negative life events had the biggest effect sizes. “Thus”, the paper notes, “both individual experiences (well-being and mood) and objectifiable factors (social activity and life events) relate to DLPFC brain mitochondrial biology.” The correlation was most notable for complex I, the largest and most upstream mitochondrial OxPhos enzyme. Psychosocial experiences accounted for 18% to 25% of the variance in the abundance of this protein. For reasons not yet fully understood, the brain is exceptionally vulnerable to complex I defects [2].”

“…Moving from proteomics to single-cell RNA sequencing enabled the researchers to take an even closer look and yielded intriguing results. The correlation between psychosocial scores and complex I was undetectable for neurons but strong for glia, the “helper” cells that facilitate proper neuronal functions, such as microglia, the brain’s resident immune cells. “This may be why chronic psychological stress and negative experiences are bad for the brain,” said Caroline Trumpff, assistant professor of medical psychology in the Department of Psychiatry at Columbia University and a lead author on the paper, “because they damage or impair mitochondrial energy transformation in the dorsolateral prefrontal cortex, the part of the brain responsible for high-level cognitive tasks.” These results do not come as a complete surprise. Scientists have already shown that in animal models, stress impairs mitochondrial function [3]. Moreover, this relationship appears to be bidirectional: the same group that authored this new study had found that differences in mitochondrial energy production capacity affect anxiety and social avoidance in rodents [4].”

“…”

Via: http://haidut.me/?p=2582

Yet another study, which not only points to the gut/endotoxin as a major cause of many chronic, degenerative diseases, but also corroborates again the role that energy production plays in pathologies such as Parkinson Disease (PD). Namely, the study below found that “gut dysbiosis” can cause deficiencies of vitamins B2 and B7, which results in the classic symptoms (e.g. muscle weakness, tremors, and poor coordination) seen in PD and that correcting those deficiencies through supplementation can be a viable therapeutic strategy. The study cites a human trial (first link below) done more than 20 years ago, showing that riboflavin supplementation (90mg daily) significantly reduced the symptoms of PD patients. While the new study does not mentioned it, there have already been several human studies with biotin for treating multiple sclerosis (MS) and Huntington disease (HD), and the mechanism of action for the benefit biotin displayed in these trials was improving mitochondrial function and OXPHOS. Riboflavin does not even need an introduction as an “energy remedy” given its main role as a precursor to the crucial energy co-factor FAD, analogous to niacinamide as a precursor to NAD+. Moreover, several studies have suggested that riboflavin is an antagonist of the endotoxin receptor TLR4, which would further validate its role in treating PD, as well as the role of endotoxin/LPS in this condition. Thus, it is quite reasonable to conclude that B2 and B7 work through correcting the energy deficiency in PD caused by the gut dysbiosis and endotoxin/LPS. Now, the new study says that the vitamin supplementation is likely to help only the subset of PD patients who have gut dysbiosis. Well, that’s a rather evasive way to saying that the B vitamin therapy may work for most PD patients since the study itself states that most PD patients experience changes in the microbiome and poor digestion decades before their official diagnosis. Finally, since it does seem that PD is yet another condition driven by energy deficiency, I don’t see why adding niacinamide (a precursor to NAD+) won’t further increase the effectiveness of this vitamin therapy.

https://www.scielo.br/j/bjmbr/a/BM4WLJBtjxF8Cx3wFsjFhKb/?lang=en

https://www.nature.com/articles/s41531-024-00724-z

https://www.sciencealert.com/parkinsons-link-to-gut-bacteria-suggests-unexpected-simple-treatment

“…Researchers have suspected for some time that the link between our gut and brain plays a role in the development of Parkinson’s disease. A new study just identified gut microbes likely to be involved and linked them with decreased riboflavin ( vitamin B2) and biotin (vitamin B7), pointing the way to an unexpectedly simple treatment that may help: B vitamins.”

“…”Supplementation of riboflavin and/or biotin is likely to be beneficial in a subset of Parkinson’s disease patients, in which gut dysbiosis plays pivotal roles,” Nagoya University medical researcher Hiroshi Nishiwaki and colleagues write in their published paper. Previous research found people with Parkinson’s disease also experience changes in their microbiome long before other signs appear.”

“…Such toxins lead to the overproduction of α-synuclein fibrils – molecules known to amass in dopamine-producing cells in the substantia nigra part of our brains, and increased nervous system inflammation, eventually leading to the more debilitating motor and dementia symptoms of Parkinson’s. A 2003 study found high doses of riboflavin can assist in recovering some motor functions in patients who also eliminated red meat from their diets. So it’s possible that high doses of vitamin B may prevent some of the damage, Nishiwaki and team propose.”

Via: http://haidut.me/?p=2580

This study is one of the most damaging piece of evidence I have seen over the last 5+ years negating the claim of mainstream medicine that estrogen is protective for the brain and the reason post-menopausal women have increased risk of dementia (of which Alzheimer’s is the most common type) is the “deficiency” of estrogen that medicine says is the defining characteristic of menopause. More specifically, the study below found that using pure estrogen receptor antagonists (e.g. Faslodex, also known as Fulvestrant, or its non-steroidal analog Elacestrant) or aromatase inhibitors (e.g. letrozole) was linked to lower risk of developing dementia across the entire expected female lifespan, with the beneficial effects of those substances being more pronounced in patients under 75 years of age. Now, the reason this study is so important and damaging to the “good estrogen” hypothesis is that prior studies with similar conclusions typically used one of the non-steroidal so-called SERM drugs (e.g. clomiphene, tamoxifen, raloxifene, etc), which have anti-estrogenic effects in some tissues but are potent estrogens in others. As such, the studies with the SERM drugs showing protective effects again dementia were always explained away by medicine as actually confirming the “benefit” of estrogen for the brain since the SERM drugs are partially estrogenic, and especially so in the brain. The is no such angle of attack possible for this study since the estrogen blockers it looked at are “pure” – i.e. they are highly selective blockers of estrogen receptors with no other known major effects. And in case medicine would try to still argue that some unknown estrogenic effect explains the benefit of those drugs, the fact that aromatase inhibitors (AI) also had protective effects pretty much seals the verdict for estrogen being a baddy. Of course, the study findings suggest other substances with anti-estrogenic effects would also likely have protective effects against dementia – i.e. all fat-soluble vitamins (A, D, E, K), aspirin, progesterone, DHT, flavones/flavanones (apigenin, naringenin, chrysin, quercetin, luteolin), etc. Curious to hear/see how medicine would respond to this study, especially considering it is published in JAMA, so it would be hard to dismiss as a fake…

Oh, one nefarious thing I noticed is that the popular press article still tries to tie progesterone in as a co-culprit. The article says the anti-estrogenic drugs mentioned in the study are used to treat breast cancer caused by “estrogen and progesterone”. So, the public might get an idea that progesterone is bad and may increase risk of dementia (or cancer), when the exact opposite is the case. Namely, the drugs mentioned in the study target exclusively estrogen and estrogen-positive cancers (not progesterone-positive cancers), and progesterone just so happens to be both an estrogen receptor antagonist and an AI. Another nefarious tactic is also seen in the study itself. It calls the clearly anti-estrogenic therapy “hormone modulating therapy” (HMT), which both avoids stating that the therapy is purely estrogen blocking in nature (in contrast to the SERM drugs) while also being targeted solely at estrogen (and not progesterone). Once again, we have science being twisted to serve Big Pharma and to avoid stating the obvious conclusion based on the study findings. Namely, estrogen is a cause of dementia/Alzhemier’s and anti-estrogenic therapy (of which progesterone is perhaps the most well-known example) is protective and possibly even therapeutic for dementias that have already set in.

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2821165

https://www.curetoday.com/view/breast-cancer-treatment-may-protect-against-dementia

“…[Hormone-modulating therapies] (HMT), such as Faslodex (fulvestrant), Orserdu (elacestrant) and Femara (letrozole) are used to treat cancers that are affected by hormones estrogen and progesterone, according to the American Cancer Society. Prior research has shown mixed results on whether HMTs increase or decrease the risk of dementias.”

https://www.sciencedaily.com/releases/2024/07/240716122709.htm

“…About two-thirds of breast cancer patients have tumors that are hormone receptor positive, meaning that they grow in response to estrogen or progesterone. For these patients, HMT can impede tumor growth by blocking hormones from attaching to these receptors. While use of HMT is linked with increased survival, there is conflicting evidence about whether it increases or decreases the risk of developing Alzheimer’s disease and related dementias (ADRD), debilitating conditions that are characterized by memory loss, changes in mood or behavior, and difficulties with thinking, problem-solving and reasoning.”

“…To calculate the risk of developing ADRD, the researchers accounted for the risk of death associated with increased age and duration of exposure to HMT. They found that while HMT use was associated with an overall decrease in the relative risk of developing ADRD, the protective effect of HMT was most pronounced in patients aged 65 through 69 and diminished with age.”

“…”Our study suggests that younger women may benefit more from HMT in terms of reduced risk of developing Alzheimer’s disease and other types of dementia,” said Cai. “The benefits of HMT decreased for women aged 75 and older, particularly in those who identified as white. This suggests that the timing of HMT initiation is crucial and treatment plans should be tailored to a patient’s age.””

Via: http://haidut.me/?p=2578

This is a study that has a lot of relevance for virtually every person living in a “developed” country. Multiple studies have documented the decrease in empathy and increase in psychopathic tendencies in Western populations over the last 2-3 decades. Despite vehement denials by mainstream medicine, there is solid evidence that elevations in extracellular serotonin can cause a drastic reduction in empathetic behavior. This makes the widespread usage of SSRI drugs a prime suspect for the reductions of empathy seen across virtually all Western countries, and virtually absent in countries where SSRI usage is low or lacking. However, the increase in pychopathic behavior/tendencies is also seen in people not taking SSRI drugs, so there is probably more than one culprit. The study below suggests that anti-anxiety drugs (the benzodiazepine class), much more widely prescribed than SSRI drugs, can also reduce empathy. To make matters worse, while SSRI and other “stronger” psychotropic drugs are still not very widely used in people under 18 years of age, that is not the case for anti-anxiety drugs, which are prescribed to even children under the age of two. Certainly not a good omen for any any society if many of its children are pharmacologically conditioned to be psychopaths from a very early age. Perhaps just as importantly, the study demonstrated that cortisol levels determine the levels of empathy. High-cortisol blocked empathetic behavior while low or moderate levels did not. So, chronic stress (resulting in chronically elevated cortisol) not only makes us physiologically sick, but also callous and psychopathic towards others. With that mind, there is little mystery as to why “developed” countries are turning into psychopathic cesspools, given that chronic and unavoidable stress (which raises both serotonin and cortisol) is with us 24×7, even if nobody was taking any drugs.

https://pubmed.ncbi.nlm.nih.gov/27375528/

https://pubmed.ncbi.nlm.nih.gov/37209151/

https://www.uchicagomedicine.org/forefront/news/2016/june/anti-anxiety-medication-limits-empathetic-behavior-in-rats

“…Rats given midazolam, an anti-anxiety medication, were less likely to free trapped companions because the drug lessened their empathy, according to a new study by University of Chicago neuroscientists. The research, published in the journal Frontiers in Psychology, validates studies that show rats are emotionally motivated to help other rats in distress. In the latest study, rats treated with midazolam did not open the door to a restrainer device containing a trapped rat, although control rats routinely freed their trapped companions. Midazolam did not interfere with the rats’ physical ability to open the restrainer door, however. In fact, when the restrainer device contained chocolate instead of a trapped rat, the test rats routinely opened the door. The findings show that the act of helping others depends on emotional reactions, which are dampened by the anti-anxiety medication. “The rats help each other because they care,” said Peggy Mason, PhD, professor of neurobiology at the University of Chicago. “They need to share the affect of the trapped rat in order to help, and that’s a fundamental finding that tells us something about how we operate, because we’re mammals like rats too.”

“…Mason and her team also tested levels of corticosterone, a stress hormone, in the rats when first exposed to the trapped cage mate and compared them to their later behavior. Those with low- to mid-level responses were most likely to free their companions later. They found that those with the highest levels of corticosterone, or those that were under the most stress from the situation, were the least likely to help their cage mates. This fits well with findings in humans suggesting that eventually high stress becomes immobilizing rather than motivating.”

Via: http://haidut.me/?p=2574

The findings of this study are particularly alarming as they suggest there are now endocrine disruptors, likely present in the majority of people, capable of causing structural changes and physical damage long before the long-term endocrine effects get a chance to accumulate and cause harm on their own. Namely, the study below found microplastics in four (4) out of five (5) male patients diagnosed with erectile dysfunction (ED). Now, as is probably obvious to all readers, these microplastics did not get lodged into the male reproductive organs directly. They got transported there by the vascular system and their origin is likely the various foods and drink we consume that were packaged in plastic containers/bags. As such, all other highly vascular organs (and especially the heart, as a study author noted) are likely to have similar accumulations of microplastics. As suggested above, putting their endocrine disrupting effects aside, those microplastics directly cause endothelial damage by physically injuring the blood vessel walls, which results in a chronic low-grade inflammation response in said vessels. That low-grade vascular inflammation is a known cause of cardiovascular disease (CVD), dementia, mental conditions, and even cancer. In some cases, if the microplastic particles are big enough, they can cause blockage of a specific vessel and lead to an ischemic event, which in the case of an organ such as the heart (e.g. heart attack) or brain (e.g. stroke), can be lethal. Unfortunately, since there is no known way to trigger the removal of those plastic particles, the only “solution” (as the study authors themselves state) is to avoid using plastics as much as possible in our daily lives. Given just this issue alone, it is little wonder there is an infertility epidemic in most “developed” countries, where the usage of plastics is ubiquitous. Those microplastics in our bodies are both chemical (through their endocrine effects) and physical (through the physical damage/blockage they cause) contraceptives, in both men and women.

https://www.nature.com/articles/s41443-024-00930-6

https://www.msn.com/en-my/health/other/microplastics-found-in-penile-tissue-raising-concerns-about-erectile-dysfunction/ar-BB1oPlJ6?item=flightsprg-tipsubsc-v1a?season//

https://www.medicalnewstoday.com/articles/microplastic-found-in-penis-infertility-sperm-count-erectile-dysfunction

“…Male infertility remains a global issue, with its causes often not well understood. Given the growing evidence of microplastics infiltrating various biological systems, such as blood and lungs, researchers are now exploring their potential effects on reproductive systems. Previous research has investigated the presence of microplastics in male reproductive organs. For example, in one study, researchers discovered 12 different types of microplastics in the testicles of dogs and humans. In dogs, they found that higher levels of certain microplastics correlated with lower sperm counts and reduced testis weight. Now, new research published in IJIR: Your Sexual MedicineTrusted Source has revealed that four out of five penis tissue samples from five men contained seven different types of microplastics. These polymer fragments can vary in size from less than 0.2 inches (5 millimeters) to as small as 1 micrometer (1/25,000th of an inch). Smaller fragments, known as nanoplastics, are measured in billionths of a meter. Microplastics form when larger plastic materials degrade chemically or wear down physically into tinier pieces.”

Via: http://haidut.me/?p=2572

One of the most widespread interventions during pregnancy is flu vaccination. Pregnant mothers are relentlessly pressured by their doctors at every visit to stay up-to-date on their flu vaccinations and it is not uncommon for mothers to receive several such vaccines during pregnancy. There has been a lingering suspicion among many doctors that flu vaccination during pregnancy is at best ineffective and at worst associated with subsequent development of both pregnancy complications for both mother and child, complications during labor, and subsequent development of chronic conditions in the child. The most infamous such hypothesis is the vaccine-autism link, even though it focuses primarily on the role of child vaccination (after birth). That is a topic for which a single blog post won’t suffice, and the point of this post is simply this – wouldn’t it be great if there was a safe, cheap and widely available remedy that the mother can use during pregnancy, instead of a flu vaccine, that can prevent the complications to both mother and child as a result of the mother contracting the flu? According to the study, the answer to that question is yes, and that simple, cheap and widely available remedy is low-dose aspirin. A human-equivalent of a baby aspirin daily fully prevented the vascular inflammation that a flu infection caused in the mother, as well as the flu-induced fetal loss. Considering that low-dose aspirin is already the best available remedy for (pre)eclampsia, it sound like aspirin is truly a “wonder” drug, at least in pregnancy. The even better news is that these findings do not apply only to flu and/or only to pregnancy. COVID-19, as well as most other viral infections, cause similar systemic state of inflammation, which affects primarily the vascular system. As such, the study below suggests that aspirin may be a viable prophylactic and treatment intervention for all other viral conditions as well.

http://dx.doi.org/10.3389/fimmu.2024.1378610

https://www.sciencedaily.com/releases/2024/07/240702200404.htm

“…A world-first study has found low-dose aspirin may treat flu-induced blood vessel inflammation, creating better blood flow to the placenta during pregnancy. Animal studies examined whether the treatment for preeclampsia could be applied to flu infections — and the results, according to the research team, were very promising. Lead researcher and RMIT Post-Doctoral Research Fellow, Dr Stella Liong, said flu infections during pregnancy can resemble preeclampsia, a pregnancy complication that causes inflammation to the aorta and blood vessels. Low-dose aspirin is commonly taken to prevent preeclampsia, as it stops the body from creating chemicals that cause inflammation. “When the vascular system is inflamed, it leads to poor blood flow and affects the aorta’s function,” she said. “This is especially a problem during pregnancy where good blood flow to the placenta is crucial to the development of the fetus.” The research, led by RMIT University in collaboration with Trinity College Dublin, Ireland Professor John O’Leary and University of South Australia Professor Doug Brooks, found fetuses and placenta from mice with influenza A were smaller than those from uninfected mice. Markers of low oxygen to the blood and poor blood vessel development were also evident in the fetuses. However, mice treated daily with low-dose aspirin had less inflammation and improved fetal development and offspring survival.”

Via: http://haidut.me/?p=2570

Despite the widespread food fortification with vitamins in many “developed” countries, the fortification mostly revolves around iron, vitamin B1 and niacin 9B3). Even if foods are fortified with other vitamins, such fortification is rare, and even when done it is invariably performed with the inactive precursors of vitamins due the lower cost of using precursors. For some of the vitamins, especially vitamins B6 and B2, multiple studies have demonstrated that administering the precursor has diminished effectiveness in aging/disease due to reduced conversion into the active form. In fact, the lack of conversion of the cheap vitamin B6 precursor (pyridoxine Hcl) is the main cause of the well-known neuropathy side effect from pyridoxine supplementation, while neuropathy does not occur when the active form of B6 is taken instead. Anyways, the study below demonstrates that a simple deficiency of the activated form of vitamin B6 – pyridoxal-5′-phosphate (P5P) – is enough to cause full blown diabetes II in animals and that, conversely, restoring the levels of P5P may be able to reverse some cases of diabetes. Now, the point of this post is not to make people immediately start popping vitamins left and right, but rather to point out that in some (many?) cases a chronic serious disease that has spun a massive medical industry around it, may be nothing more than simple nutrient deficiency resulting in suppressed mitochondrial function (as is the case in this study as well). As such, a reasonable approach would be to do some testing for P5P, as well as the activity of several of the enzymes that depend on that vitamin/cofactor. If deficiency is confirmed, then it may be safer to try first P5P supplementation instead of the myriad of pharma drugs a doctor would likely push hard on every patient newly diagnosed with diabetes II. The story Peat often told about his father curing his diabetes I by eating Brewer’s yeast (which is very rich in the B vitamins) now has a study corroborating its legitimacy.

https://dx.doi.org/10.1126/sciadv.ado4513

“…Consistent with our results in zebrafish, a pyridoxine-free diet supplemented with 4-DP caused a blunted insulin release in the pancreas of rats (51). In light of the ongoing debate, about whether vitamin B6 reduction is a cause or a consequence of diabetes (52), our data show that the former is likely true.”

https://medicalxpress.com/news/2024-07-cells-pancreas-crucial-blood-sugar.html

“…To find out what makes the first responder cells unique, the researchers compared the gene expression of highly glucose-sensitive beta cells to those that are less sensitive. They found that first responders are involved in vitamin B6 production. The first responder cells express a key enzyme involved in transforming the inactive form of dietary vitamin B6 into the form that is active in the cells. In close collaboration with Prof. Guy Rutter’s team at the University of Montreal, the researchers turned off the vitamin B6 production in both zebrafish and mouse pancreas. The ability of the beta cells to respond to high blood sugar was dramatically reduced in both species. “This indicates that vitamin B6 plays an evolutionarily conserved role in the response to glucose. It is possible that the first responders produce and supply Vitamin B6 to the rest of the beta cells to regulate their activity. Checking whether this indeed is the case is one of our next steps,” says Prof. Ninov.”

Via: http://haidut.me/?p=2567

It seems that mainstream medicine is keeping close tabs on the Peatarian community. After denying for decades that “primitive” therapies such as aspirin or the mocked “Linus Pauling Protocol” (high-dose intravenous (IV) vitamin C) have any therapeutic effects on cancer, despite reluctantly acknowledging that aspirin may prevent many/most cancers, there have been several studies published in the last year or so that are now making the bold claim that aspirin can (and should) be considered as primary therapy for cancer, or at least for solid tumors. Well, considering my own experiments showing therapeutic effects of aspirin (and B vitamins) in non-solid tumors, I think it is reasonable to claim now that aspirin can (and should) be tried as primary therapy for all types of cancer. In any event, the study below demonstrated striking reduction of tumor growth in an animal model of the invariably lethal Ehrlich ascites carcinoma (EAC) as a result of administering aspirin and/or vitamin C for just 10 days. There were 3 groups – vitamin C, aspirin, and a combination treatment group. The therapeutic effect was the strongest in the combination group, but the monotherapy groups were not far behind. The human equivalent doses were about 550mg/kg vitamin C and 8.5mg/kg daily, with vitamin C administered by injection and aspirin administered orally. There was no toxicity as a result of the administered treatments, which is in direct contradiction to current oncology dogma claiming that any curative treatment for cancer must work, by definition, through a mechanism resulting in the killing of the “mutant” and “alien” cancer cells. Now, a daily dose of 40g-50g vitamin C for a human is a lot and is not feasible to administer orally as most humans cannot absorb more than 2g-3g vitamin C daily via the oral route. That is probably why the study used intraperitoneal route for the vitamin C administration, which mimics well the IV route of the Linus protocol. Not only was this combination treatment highly beneficial for this type of tumor, but (in corroboration) the study cites another one where the same treatment protocol produced better effects for liver cancer than the established “standard of care” treatment. Interestingly, there is already a drug on the market officially approved for cancer treatment in humans, and that drug is just a combination of 5g vitamin C and 50mg vitamin K3 (menadione), administered orally. The drug’s trade name is Apatone, and since vitamin C exhibited a synergistic effects with aspirin in the current study, I suspect augmenting Apatone (maybe call it Apatone+) by adding aspirin to the already approved formulation would further improve its already striking effects on even terminal cancer cases. Also, since Apatone has already demonstrated that 5g of oral vitamin C is enough via oral route, there is no need to go for the massive vitamin C dose administered by injection, as used in this study.

https://pubmed.ncbi.nlm.nih.gov/36809998/

https://pubmed.ncbi.nlm.nih.gov/39012613/

“…A recent study by El Sadda et al. [20] discovered that a combination of ASA and AS was a well-tolerated and effective treatment for hepatocellular carcinoma (HCC) rats, surpassing the effectiveness of doxorubicin treatment; however, testing this combination’s efficacy in treating other types of tumors has still not been investigated. This study investigated the effectiveness of combining ASA and AS compared with treatment with ASA or AS alone in treating Ehrlich solid tumors in mice.”

“…At random, the mice were grouped into eight groups (10 mice each). Four of these groups included healthy mice that were not injected with any solution (Healthy); healthy mice that were treated intraperitoneally with AS (4 g/kg) once daily for 10 consecutive days (AS); healthy mice that were treated by oral gavage with ASA (60 mg/kg) once daily for 10 consecutive days (ASA); and healthy mice that were treated intraperitoneally with AS (4 g/kg) and by oral gavage with ASA (60 mg/kg) once daily for 10 consecutive days (AS+ASA). Four additional groups studied the antitumor effects of AS, ASA, and AS with ASA on tumor-bearing mice. These groups included mice that were injected with EAC cells (subcutaneously with 1×106 tumor cells/mouse into the right thigh of the hind limb) [EAC]; mice bearing solid tumors that were treated intraperitoneally with AS (4 g/kg) once daily for 10 consecutive days, 10 days after solid tumor inoculation (EAC+AS); mice bearing solid tumors that were treated using oral gavage with ASA (60 mg/kg) once daily for 10 consecutive days, 10 days after solid tumor inoculation (EAC+ASA); and mice bearing solid tumors that were treated intraperitoneally with AS (4 g/kg) and by oral gavage with ASA (60 mg/kg) once daily for 10 consecutive days, 10 days after solid tumor inoculation (EAC+AS+ASA).”

“…First, we did not record any toxicity symptoms according to administration of ASA (at a dose of 60 mg/kg) or AS (at a dose of 4 g/kg), or their combination, to healthy mice, and they did not show any significant pathological changes in all the studied parameters. In contrast, they increased antioxidant levels, and decreased MDA and NO levels, suggesting that ASA- and AS-applied doses are well-tolerated for healthy mice. Our results are in unity with Shilpi et al. [18] and Bhattacharyya et al. [27], who reported that AS and ASA are well-tolerated for therapeutic use; however, long-term use or high doses of ASA may cause oxidative stress and result in gastrointestinal erosions and apoptotic lesions [27, 28]. By tumor implantation in the right thigh of a mouse, an increase of 54.58% was recorded in the thigh dimensions in the period from day 11 to day 21 (the day of sacrifice) due to uncontrolled tumor growth. After treatment with ASA, AS, or the combination, we detected a decrease in the thigh dimensions by 2.9%, 20.53%, and 21.8%, and reductions in mean volumes of the separated tumors from mice legs by 40%, 36%, and 46%, respectively, due to tumor shrinking. Undoubtedly, as presented, the regression in solid tumors caused by treatment with the combination was superior. These observations indicate that ASA, AS, or the combination can inhibit tumor growth; however, the combination is more powerful. In 2008, Chen and colleagues found that an intraperitoneal injection of AS (4 g/kg) reduced the size of aggressive glioblastoma, pancreatic, and ovarian tumors in mice by 41–53% [29]. One of the key factors in evaluating a successful compound for fighting cancer and tumors is its ability to prolong lifespan. An increase in lifespan of at least 25% is hypothesized as an effectual antitumor response [30]. Our current research shows that ASA, AS, and their combination may help prolong lifespan and fight cancer. The untreated tumor-bearing mice had an MST of 54 days. By treatment, the MST improved to 81.5, 84, and 93.5 days, with a %ILS of 50.93%, 55.56%, and 73.15%, for ASA, AS, and the combination, respectively.”

Via: http://haidut.me/?p=2565

If there was ever any doubt that both medicine and the health of entire nations are not only unraveling, but may have collapsed years ago, this latest study should dispel any such remaining doubt. For a number of reasons. First, at the very least, the findings of the study should immediately make is abundantly clear just how fraudulent the mainstream dogma known as “genetic origins of cancer” is. We have been told for decades that cancer is just bad luck, a result of unfortunate (and random) mutations, the chance of which increases as we age. That dogma implies that mostly old people get cancer, and that was indeed the case for most of the period during which good historical medical records were kept. However, that has not been the case for the last 20+ years. I have done numerous posts over the last couple of years showing that the rates of virtually all cancers have been rapidly rising in the under-40 crowd while stabilizing (though, not declining) in the over-40 crowd. That fact alone immediately debunks the dogma of cancer as primarily a genetic mutation disease, simply because the rates of mutations in young people are much lower than in older people, as well as the fact that increasing cancer rates in the under-40 crowd across all “developed” countries are anything but “random”. In addition, no cancerous mutation could sweep through such a vast number of people (and widely dispersed territories) in just 1-2 decades. Thus, if the genetic origins of cancer hypothesis is quite clearly a scam, the only reasonable conclusion is that something absolutely terrible must have happened over the last 1-2 decades to the quality of the environment “young” people live in. The reason I put “young” in quotation marks is that based on these developments one can safely conclude that there are no more biologically young people any more, since the chronologically young not only have more rapidly rising rates of deadly diseases as the chronologically old(er) people, but are dying from those diseases at higher rates. As I said in another post of mine years ago – the young and the old have switched places.

However, as scary as those prior findings on cancer rates may be, the findings of the study below are truly devastating. Those findings prove beyond any reasonable doubt that not only is the official dogma on cancer dead-wrong, but that society/civilization as a whole has little chance of surviving if its youngest members – the future – are getting decimated by something that just a decade ago was considered a “gizzer disease”. Namely, colon cancer. When teens and even children as young as 10 are not only getting colon cancer at unprecedented rates but those rates continue to rise rapidly, then it makes little sense to even speak of “public health”, as there is clearly no such thing. Considering that colon cancer has 37%+ average mortality rate (across all stages) in adults, and that this mortality rate is now likely higher in the youngest patient groups, the findings mean that probably half of the children and teens diagnosed with colon cancer will simply die, which has absolutely devastating consequences for any country and its future, especially considering the abysmally low birth rates not only in most “developed” countries but the world as a whole. So much for the non-stop propaganda about “overpopulation”…or…maybe something more sinister is at play here.

https://www.bbc.com/news/health-53409521

Now, since cancer is quite obviously an environmentally-driven disease, even the teens and children who do not get colon cancer probably have abysmal health since they live in the same environment that caused the cancer in their peers. As such, “young” people – a country’s future – can no longer be expected to stay healthy enough to even be able to take care of themselves, let alone start families or work productive, meaningful jobs. That is exactly what most “developed” countries have been experiencing over the last 2+ decades. In such a state of society, it is little wonder that suicide and substance abuse rates are through the roof and keep rising (just like cancer rates). If the collection of fraudulent medical dogmas driving such catastrophic results are not soon confronted, exposed and de-funded, not only will the “developed” world quickly revert back to a 3rd world status, but there may not be enough healthy people left to even keep a country/society together.

https://www.cancer.gov/news-events/cancer-currents-blog/2020/colorectal-cancer-rising-younger-adults

https://doi.org/10.1016/S0016-5085(24)02668-4

https://www.health.com/study-colorectal-cancer-rates-children-teens-8648696

“…For the study, his team analyzed data from the Centers for Disease Control and Prevention (CDC) Wonder database, which offers publicly available data on mortality, cancer incidence, census data, vaccinations, and more.4 They tracked colorectal cancer incidence rates between 1999 and 2020 among people in seven different age cohorts, spanning from ages 10 to 44. Mohamed’s team found that rates rose across the board in all age groups during this time, but that younger demographics saw a sharper uptick in cases. Though the percentage increases were steepest in those between the ages of 10 and 24…”

Via: http://haidut.me/?p=2559