ApoE4 Information for Alzheimer’s, and Chronic Diseases Including PD

The Wiki page, Apoe4 offers a collection of resources and information that can help you prevent and address health problems related to APOE -ε4 allele. APOE, short for Apolipoprotein E, is both a protein and a gene. As a protein, ApoE is involved in the metabolism of fats (lipids) in the body and comes in different isoforms. In our modern environment, the ε4 allele of the gene confers a higher risk for Alzheimer’s disease and other medical conditions. It is possible to be tested to see if you carry the E4 gene which would mean you are more likely to develop Alzheimer’s, although many other factors also determine vulnerability to Alzheimer’s. E4 is also associated with other chronic diseases including dementia, brain disorders, high cholesterol, infectious diseases susceptibility, gallstones, and cardiovascular disease.

Source: ApoE4.Info Wiki

Review of Possible Use of a Keto Diet in PD Treatment

A review focused on the role of ketogenic diets in neurodegenerative diseases (including PD) was published in the MDPI journal Nutrient in 2019. The goal of the review was to assess the effectiveness of ketogenic diets as part of therapy for neurodegenerative diseases. In PD, dopaminergic neurons in the substantia nigra are affected by a degeneration process leading to motor and non-motor disturbances. The available results of research projects dealing with the use of the KD and ketone bodies in neurodegenerative diseases are fairly promising. At the same time, the majority of studies reviewed were employed in vitro or by using animal models. The number of studies with human participation is rather small, and those that exist feature relatively short therapy duration periods.

Source: Role of Ketogenic Diets in Neurodegenerative Diseases (Alzheimer’s Disease and Parkinson’s Disease)

Fact Sheet: Dietary Supplements for Primary Mitochodrial Disorders

NIH publishes a fact sheet for health professionals on dietary supplements for primary mitochondrial disorders. The fact sheet summarizes published scientific trials, other studies, and reports on the use of dietary supplements to treat primary mitochondrial disorders. The most common ingredients in dietary supplements used in PMD therapy include vitamin C, vitamin E, and alpha-lipoic acid; electron donors and acceptors, such as CoQ10and riboflavin; compounds that can be used as alternative energy sources, such as creatine; and compounds that can conjugate or bind mitochondrial toxins, such as carnitine. A combination of these products is commonly called a mitochondrial cocktail. However, there are many combinations and dosages so the term is nonspecific and nondescriptive. Drug interaction needs to be taken into consideration as well as the level of evidence of efficiency, quality of ingredients, and dosage.

Source: Dietary Supplements for Primary Mitochondrial Disorders – Health Professional Fact Sheet

Review: The Role of Dietary Fat in Treatment of Brain Diseases

A review published in the Current Neuropharmacology journal in 2018 looked at the impact of dietary fats on brain function. It also examined gut-brain communication through microbiota; the impact of probiotics and prebiotics on brain functions; SCFA’s, microbiota, and neuroinflammation. It reviewed lipid sensing, satiety, and processing of hedonic food; the impact of diet on the hypo-thalamic control of reproduction; neuroprotective effects of N-3 PUFAs; dietary PUFAs, brain PUFAs and the role of PUFAs. The results of this review revealed that dietary fats are both friends and foes for brain functions. However, dietary manipulation for the treatment of brain disorders is not just a promise for the future, but a reality. In fact, the clinical relevance of the manipulation of dietary lipids, as for KDs, is well-known and currently in use for the treatment of brain diseases.

Source: Impact of Dietary Fats on Brain Functions
LGIT safe (see 305)

Whole Food Plant-Based Nutrition and Cardiovascular Disease

A review by Caldwell B. Esselstyn published in the Journal of Geriatric Cardiology in 2017 covered the connection between a plant-based diet and coronary artery disease. Caldwell states that in ignoring diet as a cause of CVD there is no hope for a cure as patients continue to consume the foods that destroy them. He discusses studies conducted using WFPBN in patients ill with CAD. The results showed that WFPBN can halt and reverse CVD. In summary, current palliative cardiovascular medicine consisting of drugs, stents, and bypass surgery cannot cure or halt the vascular disease epidemic and is financially unsustainable. WFPB can restore the ability of endothelial cells to produce nitric oxide, which can halt and reverse disease without morbidity, mortality, or added expense.

Source: A plant-based diet and coronary artery disease: a mandate for effective therapy – Coldwell

Suporting Articles:

Diet for Heart Health

A study by Caldwell published by the NIH set out to show that plant-based nutrition helps prevent coronary artery disease in a large group of patients. 198 patients with CVD were followed and given counseling on how to convert from a regular diet to plant-based nutrition. Results showed that 89% adhered to the diet and in the group of adherent participants major cardiac events recurred at a rate of 0.6%. This was significantly less than reported in other similar studies where a smaller group was used. Of the non-adherent participants, 62% experienced adverse events. Caldwell concludes that patients with CVD respond to intense counseling and when on a sustained plant-based diet for a mean 3.7 years they experience a low rate of cardiac events. Plant-based nutrition has the potential for a large effect on the CVD epidemic.

Source: A Way to Reverse CAD?

Supporting Articles: Evidence listed by Coldwell to support a low-fat vegan diet:

2020 Clinical Trial: Mannitol for PD

The NIH Clinical Trial published information on a study provided by Arkadir David of the Hadassah Medical Organization. The study took 60 participants and ran a phase II single center, randomized, double blind and placebo controlled study assessing the safety, tolerability, and effects of progressively increased dose of oral mannitol in PD. The study began in November 2018 and will end in December 2020. There were 60 Participants of both genders and aged 40 to 75 years. The study assessed the safety of mannitol by the number of treatment-related adverse events and significant changes in vital signs. Tolerability was tested by the level of discomfort. Other changes in participants that were monitored included changes in constipation assessment; Montreal Cognitive Assessment; Brief Smell Identification; change in levodopa-equivalent dose units; change in non-motor symptoms of PD scale and the change in the ratio of total-to-proteinase K-resistant a-syn in red blood cells measured by enzyme-linked immunosorbent assay. Results of this study have not yet been posted.

Source: Safety, Tolerability and Effects of Mannitol in Parkinson’s Disease – Full Text View – ClinicalTrials.gov

 

Nattokinase as a Possible Treatment for Cardiovascular Disease

A 2018 review in the NCBI Biomarker Insights journal looks at nattokinase as a possible alternative in the prevention and treatment of cardiovascular disease. Nattokinase (NK), the most active ingredient of natto (cheese-like food made from fermented soybeans), possesses a variety of favorable cardiovascular effects. The review looks at the pharmacological effects and mechanisms of NK in terms of fibrinolytic/antithrombotic effects, anti-atherosclerotic and lipid-lowering effects, antihypertensive effects, antiplatelet/anticoagulant effects, and neuroprotective actions. The review also lists the few clinical studies that have been done with NK. NK is registered as a nutritional supplement and not a drug. In summary, compared with traditional antithrombotic and antihypertensive drugs, NK is characterized by high safety, low cost, simple production process, oral availability, and long in vivo half-life. As such, it is expected to become a new-generation drug for thrombotic disorders or CVDs.

Source: Nattokinase: A Promising Alternative in Prevention and Treatment of Cardiovascular Diseases

Food/Drug/Supplements that effect INR

Common drugs that can interact with warfarin include:

Aspirin or aspirin-containing products
Acetaminophen (Tylenol, others) or acetaminophen-containing products
Antacids or laxatives
Many antibiotics
Antifungal medications, such as fluconazole (Diflucan)
Cold or allergy medicines
Ibuprofen (Advil, Motrin IB, others) or naproxen sodium (Aleve, Naprelan, others)
Medications that treat abnormal heart rhythms, such as amiodarone (Pacerone, Nexterone)

scan for more information on drug interaction:


drug interactions with Warfarin

www.ncbi.nlm.nih.gov/pmc/articles/PMC1942100/bin/18TT1.jpg
drugs that interact with warfarim

Common supplements that can interact with warfarin include:

Vitamin K
Vitamin K2 [2]
Vitamin C [3]
Probiotics [2]

Resveratrol (possibly safe, see [1])
Omega 3
Coenzyme Q10 (ubiquinone)
Dong quai
Garlic
Ginkgo biloba
Ginseng
Green tea
St. John’s wort
Vitamin E
Vitamin A
Senna leaves
Flavonoids – safe [4]
Nattokinase
Vitamin D3 – reduce vitamin K

Take Magnesium/Zinc/Iron at least two hours apart from Warfarin That should eliminate any possible interaction.

Common foods and drinks that might interact with warfarin include:

Food high in Vitamin K (green leafy vegetables)*

Cranberries or cranberry juice
Grapefruit
Alcohol
Garlic
Black licorice

It’s important to have a consistent amount of vitamin K in your diet (if on warfarin). If you have little vitamin K in your diet, a sudden spike can increase your risk of bleeding.

Resistance to oral anticoagulants has been associated with high vit K food intake.

Foods rich in vitamin K include:

beef liver, broccoli, Brussels sprouts, cabbage, collard greens, endive, kale, lettuce, mustard greens, parsley, soy beans, spinach, Swiss chard, turnip greens, watercress, and other green leafy vegetables.

Moderate to high levels of vitamin K: asparagus, avocados, dill pickles, green peas, green tea, canola oil, margarine, mayonnaise, olive oil, and soybean oil. Snack foods containing the fat substitute,

olestra, are fortified with 80 mcg of vitamin K per each one ounce serving

Consumption of large amounts of mango fruit has been associated with enhanced effects of warfarin. The exact mechanism of interaction is unknown but may be related to the vitamin A content, which may inhibit metabolism of warfarin.

Limited data also suggest a potential interaction between warfarin and cranberry juice resulting in changes in the INR and/or bleeding complications.

There have been several case reports in the medical literature of patients consuming grapefruit, grapefruit juice, or grapefruit seed extract who experienced increases in INR. R(+) warfarin…possibly safe

.. elevated INR due to pomegranate juice

Black currant juice and black currant seed oil may theoretically increase the risk of bleeding or bruising if used in combination with anticoagulants.

Soy protein in the form of soy milk was thought to be responsible for a case of possible warfarin antagonism in an elderly male stabilized on warfarin. The exact mechanism of interaction is unknown, as soy milk contains only trace amounts of vitamin K. Subtherapeutic INR values were observed approximately 4 weeks after the patient began consuming soy milk daily for the treatment of hypertriglyceridemia. No other changes in diet or medications were noted during this time. The patient’s INR returned to normal following discontinuation of the soy milk with no other intervention.

An interaction with chewing tobacco was suspected in a case of warfarin therapy failure in a young male who was treated with up to 25 to 30 mg/day for 4.5 years. The inability to achieve adequate INR values led to eventual discontinuation of the chewing tobacco, which resulted in an INR increase from 1.1 to 2.3 in six days. The authors attributed the interaction to the relatively high vitamin K content in smokeless tobacco.

Some experts recommend that continuous enteral nutrition should be interrupted for one hour before and one hour after administration of the anticoagulant dose and that enteral formulas containing soy protein should be avoided. Anticouglant users should consider limiting the consumption of cranberry juice or other cranberry formulas or pomegranate juice, black currant juice, and black currant seed oil.

<h2) Natural blood thinners</H2
Celery, galic, vit C
are does Warferin alternativesss,
need some postapocaliptiiic solution, assumin, only

Other blood thinning medication:

Plavix – avoid grapefruits, Celery
לתרופות החדשות למניעת קרישה (קסרלטו, אליקוויס ופרדקסה) כמעט שאין התנגשויות ידועות עם מזון.
avoid grapefruits, Celery, garlic

לבני ממליצה גם להיזהר ממזונות מדללי דם כמו סלרי ושום ולא לצרוך אותם בכמויות גדולות, למרות שכרגע אין מידע על אינטראקציות של מזונות אלה עם התרופות החדשות.

References:

www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/in-depth/warfarin-side-effects/art-20047592

[1] www.ncbi.nlm.nih.gov/pmc/articles/PMC5090816/

[2] 1.getmanaged.online/gut-bacteria-and-probiotics-that-lower-inr/

[3] Vitamin C
Vitamin C with Rose Hips (ascorbic acid)

Ascorbic acid has been implicated in causing warfarin resistance. However, controlled clinical trials have not demonstrated clinically important variations in prothrombin times. The possibility of an interaction may be considered if warfarin resistance is encountered in patients taking high doses of ascorbic acid.
References
Smith EC, Skalski RJ, Johnson GC, Rossi GV “Interaction of ascorbic acid and warfarin.” JAMA 221 (1972): 1166
Hume R, Johnstone JM, Weyers E “Interaction of ascorbic acid and warfarin.” JAMA 219 (1972): 1479
Rosenthal G “Interaction of ascorbic acid and warfarin.” JAMA 215 (1971): 1671
Weintraub M, Griner PF “Warfarin and ascorbic acid: lack of evidence for a drug interaction.” Toxicol Appl Pharmacol 28 (1974): 53-6
Feetam CL, Leach RH, Meynell MJ “Lack of a clinically important interaction between warfarin and ascorbic acid.” Toxicol Appl Pharmacol 31 (1975): 544-7

[4] = flavonoids, no interaction with Warfarin – www.ncbi.nlm.nih.gov/pubmed/28696372qqqq

****************

Guo LQ, Yamazoe Y “Inhibition of cytochrome P450 by furanocoumarins in grapefruit juice and herbal medicines.” Acta Pharmacol Sin 25 (2004): 129-36
Bodiford AB, Kessler FO, Fermo JD, Ragucci KR “Elevated international normalized ratio with the consumption of grapefruit and use of warfarin.” SAGE Open Med Case Rep 0 (2013): 1-3
Suvarna R, Pirmohamed M, Henderson L “Possible interaction between warfarin and cranberry juice.” BMJ 327 (2003): 1454
Beckey NP, Korman LB, Parra D “Effect of the moderate consumption of olestra in patients receiving long-term warfarin therapy.” Pharmacotherapy 19 (1999): 1075-9
Kempin SJ “Warfarin resistance caused by broccoli.” N Engl J Med 308 (1983): 1229-30
Sullivan DM, Ford MA, Boyden TW “Grapefruit juice and the response to warfarin.” Am J Health Syst Pharm 55 (1998): 1581-3
Westfall LK “An unrecognized cause of warfarin resistance.” Drug Intell Clin Pharm 15 (1981): 131
Harrell CC, Kline SS “Vitamin K-supplemented snacks containing olestra: Implication for patients taking warfarin.” Jama J Am Med Assn 282 (1999): 1133-4
Walker FB “Myocardial infarction after diet-induced warfarin resistance.” Arch Intern Med 144 (1984): 2089-90
Pedersen FM, Hamberg O, Hess K, Ovesen L “The effect of dietary vitamin K on warfarin-induced anticoagulation.” J Intern Med 229 (1991): 517-20
Grant P “Warfarin and cranberry juice: an interaction?” J Heart Valve Dis 13 (2004): 25-6
Griffith LD, Olvey SE, Triplett WC “Increasing prothrombin times in a warfarin-treated patient upon withdrawal of ensure plus.” Crit Care Med 10 (1982): 799-800
Ge B, Zhang Z, Zuo Z “Updates on the clinical evidenced herb-warfarin interactions.” Evid Based Complement Alternat Med 2014 (2014): 957362
Kazmier FJ, Spittell JA Jr “Coumarin drug interactions.” Mayo Clin Proc 45 (1970): 249-55
Wells PS, Holbrook AM, Crowther NR, Hirsh J “Interactions of warfarin with drugs and food.” Ann Intern Med 121 (1994): 676-83
Agencia Española de Medicamentos y Productos Sanitarios Healthcare “Centro de información online de medicamentos de la AEMPS – CIMA. Available from: URL: cima.aemps.es/cima/publico/home.html.” ([2018]):
Zallman JA, Lee DP, Jeffrey PL “Liquid nutrition as a cause of warfarin resistance.” Am J Hosp Pharm 38 (1981): 1174
Watson AJ, Pegg M, Green JR “Enteral feeds may antagonise warfarin.” Br Med J 288 (1984): 557
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Griffiths AP, Beddall A, Pegler S “Fatal haemopericardium and gastrointestinal haemorrhage due to possible interaction of cranberry juice with warfarin.” J R Soc Health 128 (2008): 324-6
Parr MD, Record KE, Griffith GL, et al “Effect of enteral nutrition on warfarin therapy.” Clin Pharm 1 (1982): 274-6
Chow WH, Chow TC, Tse TM, Tai YT, Lee WT “Anticoagulation instability with life-threatening complication after dietary modification.” Postgrad Med J 66 (1990): 855-7
Hamann GL, Campbell JD, George CM “Warfarin-cranberry juice interaction.” Ann Pharmacother 45 (2011): e17
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Brandin H, Myrberg O, Rundlof T, Arvidsson AK, Brenning G “Adverse effects by artificial grapefruit seed extract products in patients on warfarin therapy.” Eur J Clin Pharmacol 63 (2007): 565-70
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Vitamin D | Linus Pauling Institute | Oregon State University

n a randomized, double-blind, placebo-controlled study, 112 PD patients (mean age, 72 years) on standard PD treatment were supplemented with 1,200 IU/day of vitamin D or a placebo for 12 months. Vitamin D supplementation nearly doubled serum 25-hydroxyvitamin D concentration (from mean of 22.5 ng/mL to 41.7 ng/mL) in supplemented subjects and limited the progression of PD, as indicated by a greater proportion of patients who showed no worsening (as assessed by the Hoehn and Yahr stage and the United Parkinson Disease Rating Scale part II) in the supplemented group compared to the placebo group (243). It is not known whether vitamin D insufficiency has a role in the pathogenesis of the disease, but the repletion of vitamin D may provide health benefits that go beyond the prevention and/or the treatment of PD. For example, vitamin D deficiency may contribute to the increased risk of osteoporosis and bone fracture in individuals with neurologic disorders, including PD and multiple sclerosis (244-246). Interestingly, sunlight exposure was found to be associated with improved vitamin D status, higher bone mineral density of the second metacarpal bone, and lower incidence of hip fracture in a prospective study conducted in 324 elderly people with PD (247).

Source: Vitamin D | Linus Pauling Institute | Oregon State University

All About mTOR, mTOR Inhibitors and mTOR Activators

SelfHacked published an article by Puya Yazdi, MD in September 2020 about mTOR and natural mTOR inhibitors and activators. mTOR responds to signals from nutrients, growth factors and cellular energy status and controls cell growth and proliferation based on regulating protein syntheses. mTOR is one of those things that’s good to have cycled. Sometimes we want to increase it to grow muscle and improve certain aspects of cognition, while the rest of the time we want to have low levels to increase longevity, decrease the risk of cancer, and reduce inflammation. Too much mTOR activation is associated with many diseases including neurodegeneration. There are mTOR inhibitors mainly used as immunosuppressants to prevent transplant rejection and in anticancer therapy and strategies such as ketogenic diets. mTOR activators include a variety of amino acids and the hormone insulin as well as proteins, excess carbs, Orexin, and more. For health and longevity, we’d want systemic mTOR levels to be low most of the time, with occasional periods of activation. Research suggests it’s preferable to have mTOR more active in your brain and muscles rather than in your fat cells and liver. Exercise is ideal because it does exactly this.

Source: All About mTOR + Natural mTOR Inhibitors & Activators – SelfHacked

early puberty & EDC – endocrine disraptors

MedicalMedia.co.il דף ראשי: שער הכניסה של הרופאים לאינטרנט, חיפוש מידע רופאי מושכל, חיפוש תרופות מושכל, כתבי עת רפואיים, כינוסים, ספרייה רפואית וכל המידע שלו זקוק הרופא נמצא ב MedicalMedia

Source: Israeli Journal of Pediatrics – התבגרות מינית: מה התחדש בעשורים האחרונים?

New treatments for PD, in trials

direct administration to the brain (that’s new) of GDNF  (also new)

The FDA granted approval of Nourianz to Kyowa Kirin, Inc.

  • A universal feature of Parkinson’s is aggregation, or clumping, of the protein alpha-synuclein in the brains and body cells of people with the disease (similar to the amyloid clumps seen in Alzheimer’s disease). Multiple drug companies are conducting clinical trials to try to prevent or break up synuclein clumps, which scientists believe could stop PD in its tracks.
  • Several potentially disease-modifying therapies continue to advance via “repurposing” — scientifically evaluating drugs approved for various conditions for their benefit in PD. Isradipine (a hypertension drug) and inosine (an antioxidant supplement) are now in Phase III trials. The field also has seen promise in the diabetes drug exenatide and the cancer drug nilotinib.

New meds, in trial