Role of Vitamins in Neurodegenerative Diseases: A Review

https://pubmed.ncbi.nlm.nih.gov/34802410/

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity.”

Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington’s disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington’s disease disrupts the synthesis of acetylcholine and hormones in the brain.”

Kumar RR, Singh L, Thakur A, Singh S, Kumar B. Role of Vitamins in Neurodegenerative Diseases: A Review. CNS Neurol Disord Drug Targets. 2021 Nov 19. doi: 10.2174/1871527320666211119122150. Epub ahead of print. PMID: 34802410.

Physical Exercise as a Preventive or Disease-Modifying Treatment of Dementia and Brain Aging – Mayo Clinic Proceedings

Physical Exercise as a Preventive or Disease-Modifying Treatment of Dementia and Brain Aging – Mayo Clinic Proceedings

Mayo
Clinic Proceedings

September
2011 Volume 86, Issue 9, Pages 876–884
Physical
Exercise as a Preventive or Disease-Modifying Treatment of Dementia and Brain
Agin

http://www.mayoclinicproceedings.org/article/S0025-6196(11)65219-1/fulltext

Abstract:

A rapidly growing literature strongly suggests that exercise, specifically aerobic exercise, may attenuate cognitive impairment and reduce dementia risk. We used PubMed (keywords exercise and cognition) and manuscript bibliographies to examine the published evidence of a cognitive neuroprotective effect of exercise. Meta-analyses of prospective studies documented a significantly reduced risk of dementia associated with midlife exercise; similarly, midlife exercise significantly reduced later risks of mild cognitive impairment in several studies. Among patients with dementia or mild cognitive impairment, randomized controlled trials (RCTs) documented better cognitive scores after 6 to 12 months of exercise compared with sedentary controls. Meta-analyses of RCTs of aerobic exercise in healthy adults were also associated with significantly improved cognitive scores. One year of aerobic exercise in a large RCT of seniors was associated with significantly larger hippocampal volumes and better spatial memory; other RCTs in seniors documented attenuation of age-related gray matter volume loss with aerobic exercise. Cross-sectional studies similarly reported significantly larger hippocampal or gray matter volumes among physically fit seniors compared with unfit seniors. Brain cognitive networks studied with functional magnetic resonance imaging display improved connectivity after 6 to 12 months of exercise. Animal studies indicate that exercise facilitates neuroplasticity via a variety of biomechanisms, with improved learning outcomes. Induction of brain neurotrophic factors by exercise has been confirmed in multiple animal studies, with indirect evidence for this process in humans. Besides a brain neuroprotective effect, physical exercise may also attenuate cognitive decline via mitigation of cerebrovascular risk, including the contribution of small vessel disease to dementia. Exercise should not be overlooked as an important therapeutic strategy.

Vitamin D and the risk of dementia and Alzheimer disease

Vitamin D and the risk of dementia and Alzheimer disease


Conclusion: Our results confirm that vitamin D deficiency is associated with a substantially

increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate
about the role of vitamin D in nonskeletal conditions.

Neurology® 2014;83:1–9

Reversal of cognitive decline: A novel therapeutic program

Reversal of cognitive decline: A novel therapeutic program

Bredesen DE. Reversal of cognitive decline: A novel therapeutic program.Aging (Albany NY) 2014;6(9):707-717.

In the absence of effective prevention and treatment, the prospects for the future are of great concern, with 13 million Americans and 160 million globally projected for 2050, leading to potential bankruptcy of the Medicare system.”


Recent estimates suggest that AD has become the third leading cause of death in the United States”

Neurodegenerative disease therapeutics has been, arguably, the field of greatest failure of biomedical therapeutics development.”


In the case of Alzheimer’s disease, there is not a single therapeutic that exerts anything beyond a marginal, unsustained symptomatic effect, with little or no effect on disease progression. Furthermore, in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one.”


Patient one: 

A 67-year-old woman presented with two years of progressive memory loss.


(1) She eliminated all simple carbohydrates, leading to a weight loss of 20 pounds; 

(2) She eliminated gluten and processed food from her diet, and increased vegetables, fruits, and non-farmed fish; 

(3) in order to reduce stress, she began yoga, and ultimately became a yoga instructor; 

(4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day; 

(5) she took melatonin 0.5mg po qhs; 

(6) she increased her sleep from 4-5 hours per night to 7-8 hours per night; 

(7) she took methylcobalamin 1mg each day; 

(8) she took vitamin D3 2000IU each day; 

(9) she took fish oil 2000mg each day; 

(10) she took CoQ10 200mg each day; 

(11) she optimized her oral hygiene using an electric flosser and electric toothbrush; 

(12) following discussion with her primary care provider, she reinstated HRT (hormone replacement therapy) that had been discontinued following the WHI report in 2002; 

(13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime; 

(14) she exercised for a minimum of 30 minutes, 4-6 days per week.

Patient History, evaluation Diagnosis Status
67F 3/3 2yr memory [down double arrow]; FH+ aMCI Normal x 2.5 yrs; working

”The positive results reported here are perhaps not surprising given that therapeutic programs have proven more effective than monotherapeutics in multiple chronic illnesses, such as atherosclerotic cardiovascular disease, HIV, and cancer [535]. Indeed, chronic illnesses may be more amenable to therapeutic systems than to monotherapeutics.”




Jeff Volek – The Many Facets of Keto-Adaptation: Health, Performance

01:14 – Jeff Volek have been study Low Carbbohydrate Diets for about 15 years (since about 1998)

02:17 – Why don’t these diets get more publicity
03:35 – Sweden Becomes First Western Nation to Reject Low-fat Diet Dogma in Favor of Low-Carb High-fat Nutrition
  • 16’000 studies was reviewed  over a 2 year period
05:37 – The Problem
  • 1/3 of Americans are Obese
  • 200 Billion Dollars are spent annually on Obesity
     
06:00 – Exercise and Weight loss:
  • Small but very, very controlled Study
  • Twins exercise twice a day
11:55 – Personalized Nutrition… Where to start
  • Carbohydrate
    • Insulin control access to the fat cells, Insulin is tied to carbohydrates
15:25 – about 200 Kcal/day extra in Carbohydrate
16:00 – Total Sugar in the blood stream at any moment, Answer: 8 Grams or 2 teaspoons
17:40 – Lipogenesis (lipogenesis the formation of fat from non fat sources)
Lipogenesis is the process by which acetyl-CoA is converted to fatty acids
18:45 – Insulin Resistance = Carbohydrate Intolerance
  • Diabetes = Side Effect of Consuming too Much Carbohydrate relative to a Person’s Tolerance
21:50 – The A to Z Study (Gardner et al. JAMA 2007)
22:20 – Carbohydrate Metabolism Vs Fat-based Metabolism
  • Fatty Acid / Ketone Metabolism
    • Regression of cancer tumours
    • Life Extension
    • Reduce Oxidative Stress
    • More or Less Anti Aging
24:45 – Insulin is the most Important Physiological inhibition of lipolysis
26:00 – Ketosis and the Brain
  • when in Ketosis 50% of the brain’s energy comes from Ketones
  • when in Ketosis 40% of the brain’s energy comes from Glucose
  • when in Ketosis 10% of the brain’s energy comes from Acetoacetate
  • The brain uses about 600 kcal/day
28:25 – Ketone Terminology
  • Ketones
  • Ketosis
  • Nutritional Ketosis
  • Ketoacidosis
  • Keto adaptation
     
  • Unless you are Type 1 diabetic you don’t have to worry about Ketoacidosis
29:48 – The Ketone Zone
30:55 – Keto-adaptation dramatically alters the hypoglycemic threshold
32:20 – Ketones don’t generate as many free radicals
34:50 – Science of Low Carbohydrate Diets
35:25 – Low carbohydrate diets are more likely to affect global improvement in markers associated with metabolic syndrome (Forsythe et al. 2008)
  • Body Mass
  • Ab Fat
  • TG (Triglycerides)
  • TG AUC
  • HDL
  • TG/HDL
  • ApoB/ApoA-1
  • Small LDL
  • Glu
  • Insulin
  • HOMA
  • Leptin
  • Total SFA
37:15 – Dietary Saturated Fat and Heart Disease
  • No correlation
  • if you replace the fat with Carbohydrate the risk Increases for Heart Disease
38:50 – Plasma Saturated fat Predicts Heart Disease
40:00 – Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation (Lipids. 2008 Jan;43(1):65-77. Epub 2007 Nov 29.)
  • Despite being higher in Saturated Fat, a Low Carbohydrate diet decreased circulating levels of SFA
41:30 – On a Low Carbohydrate diet the Saturated fat is digested into Co2 (Carbon dioxide) and H20 (Water)
  • The effect of Dietary Saturated fats are are highly dependent on the carbohydrate that you eat with the fat
  • Dietary Saturated fat has very little to do with Correlation with Plasma levels of saturated fat (fat stored on the body)
42:30 – With Ketogenic Diet you can Prevent and reverse Type 2 Diabetes. Middle east has the highest rates of Diabetes, almost twice the rate of America
43:20 – Ketogenic Diet and Cancer
44:17 – Ketogenic diet as a treatment paradigm for diverse neurological disorders
  • Epilepsy
  • Aging
  • Alzheimer’s Disease
  • Parkinson’s Disease
  • Mitochondrial Disorders
  • Brain Trauma
  • Autism
  • Migraine
  • Depression
  • Wound Healing
45:50 – Tim Olsen Wins 2012 Western State 100 with time 14 hours 46 minutes (track record)
46:25 – F.A.S.T.E.R (Fat Adapted Substrate oxidation in Trained Elite Runners)
47:41 – Peak Fat Burning (grams/minute) maximum value was believed to be 1.0

  • High level Ketogenic athlete performs, 1.8 grams/minute (Off the chart, the chart only goes to 1.2 science 1.0 is Maximum)