Does Vitamin D Slow Cellular Aging?

 Why you want longer telomeres, except for this research.

Long telomeres may heighten cancer risks May 2023

You'll want your competent? doctor to step in here. I'm not medically trained so don't listen to me.

• telomeres (17 posts to November 2012)

• telomere caps (1 post to January 2022)

• telomere length (3 posts to April 2022)

Does Vitamin D Slow Cellular Aging?

We’ve long known that vitamin D plays a central role in bone health, immune function, and mood regulation. But new research suggests it may also help defend against one of aging’s most fundamental processes: the shortening of telomeres.

A newly published study from the VITAL trial, one of the largest and most rigorous supplement trials to date, found that four years of daily vitamin D3 supplementation slowed the rate of telomere shortening in adults over age 50. The findings point to a potential role for vitamin D in preserving cellular health and supporting healthy aging.

The Study: Vitamin D and Telomere Protection

Telomeres are protective end caps at the ends of chromosomes that help maintain DNA stability during cell division. Over time, telomeres naturally shorten due to aging and stress, which can lead to cell dysfunction, chronic

[in-fluh-mey-shuhn] noun

Your body’s response to an illness, injury or something that doesn’t belong in your body (like germs or toxic chemicals).

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inflammation, and an increased risk of age-related disease.

The VITAL Telomere study included 1,031 participants (average age 65) who received either:

• 2,000 IU/day of vitamin D3(If this is one of those large pills, I can't do it in one pill.)
• 1 gram/day of marine omega-3 fatty acids
• Both
• Or a placebo

People had their leukocyte telomere length (LTL) measured at baseline, year 2, and year 4 using a high-precision PCR method.

Key findings:

• Those taking vitamin D3 experienced 140 base pairs less telomere loss over 4 years compared to placebo (Each time a cell divides, bases are lost from the ends of the telomeres on each chromosome.)
• On average, telomere length in the vitamin D group was 0.035 kilobases longer per year.
• Omega-3 supplementation showed no significant impact on telomere length.

The researchers concluded that daily vitamin D3 may have an anti-cellular aging effect by reducing telomere attrition, especially when taken consistently over multiple years.

Why This Matters for Super Agers

Telomeres aren’t just a marker of age; they’re a mechanism. Shortened telomeres have been linked to heart disease, cancer, Alzheimer’s, diabetes, and more.

While telomere length is influenced by genetics, it’s also shaped by lifestyle, including stress levels, diet, physical activity, and nutrient status. The VITAL trial adds vitamin D3 to the short list of interventions with randomized, placebo-controlled evidence showing an effect on telomere preservation.

For Super Agers focused on staying biologically younger for longer, this matters. Preserving telomere length could mean preserving vitality.

Should You Take Vitamin D3 For Longevity?

This study isn’t a call to mega-dose vitamin D; it’s about long-term, moderate, consistent use under medical supervision. The study authors say: “Our findings that vitamin D supplementation preserved telomere length in the VITAL trial suggest a promising role for vitamin D in slowing a pathway for biological aging and age-related chronic disease. We believe that replication of these results in a separate randomized trial will be important before changing general guidelines for vitamin D intake.” In the meantime, here’s what you can do:

1. Ask Your Doctor About Vitamin D Testing

Vitamin D levels vary based on sun exposure, age, skin tone, and other factors. Blood testing (25-hydroxyvitamin D) can determine if supplementation is appropriate.

2. If Recommended, Stay Consistent

The telomere benefit in this study was observed after four years of daily vitamin D supplementation, not short-term use. Consistency matters.

3. Don’t Rely on Omega-3s for This Particular Benefit

While marine omega-3 fatty acids are beneficial for heart and brain health, this study did not find evidence that they preserve telomeres.

4. Layer Vitamin D with Other Longevity Habits

Telomere health is multifactorial. Combine supplementation with:

• Regular strength training
• Quality sleep cycles
• Anti-inflammatory diet
• Stress management

At the cellular level, telomere length is one of the clearest indicators of biological wear and tear. This new study shows that daily vitamin D3, at a safe, research-backed dose, may help preserve telomere length over time.

That doesn’t mean vitamin D is a magic bullet. But it’s a low-cost, low-risk intervention that might buy your cells a little more time.

The information provided in this article is for educational and informational purposes only and is not intended as health or medical advice. Do not use this information to diagnose or treat any health condition. Always consult a qualified healthcare provider regarding any questions you may have about a medical condition or health objectives. Read our disclaimers.

The Effect of Vitamin D Supplementation on Functional Outcomes in Patients Undergoing Rehabilitation After an Ischemic Stroke: A Prospective, Single-Blind, Randomized, Placebo-Controlled Study

 Your competent? doctor has known of this for years. What was done? NOTHING? So, you don't have a functioning stroke doctor, do you?

vitamin D3 (6 posts to June 2013)

The latest here:

The Effect of Vitamin D Supplementation on Functional Outcomes in Patients Undergoing Rehabilitation After an Ischemic Stroke: A Prospective, Single-Blind, Randomized, Placebo-Controlled Study            

                                 by

Wojciech Borowicz

¹,

Lucyna Ptaszkowska

²,

Rafał Małecki

^3,4 and

Małgorzata Paprocka-Borowicz

^5,6,*

¹

Department of Pediatric Infectious Diseases, Wroclaw Medical University, 50-368 Wroclaw, Poland

²

Institute of Health Sciences, University of Opole, 45-060 Opole, Poland

³

Department of Non-Procedural Clinical Science, Faculty of Medicine, Wroclaw University of Science and Technology, 51-377 Wroclaw, Poland

⁴

Department of Internal Medicine with Angiology Subdivision, Regional Specialist Hospital in Wroclaw, 51-124 Wroclaw, Poland

⁵

Division of Clinical Physiotherapy and Rehabilitation, University Centre of Physiotherapy and Rehabilitation, Faculty of Physiotherapy, Wroclaw Medical University, 50-368 Wroclaw, Poland

⁶

Department of Neurological Rehabilitation, Regional Specialist Hospital in Wroclaw, 51-128 Wroclaw, Poland

^*

Author to whom correspondence should be addressed.

J. Clin. Med. 2025, 14(6), 1848; https://doi.org/10.3390/jcm14061848

Submission received: 13 January 2025 / Revised: 25 February 2025 / Accepted: 6 March 2025 / Published: 9 March 2025

(This article belongs to the Special Issue Advances in Rehabilitation Care for Geriatric Diseases)

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Versions Notes

Abstract

Background/Objectives: 

A vitamin D deficiency is prevalent in post-stroke patients and may impair neurological recovery. While observational studies highlight the neuroprotective role of vitamin D, there is limited evidence from interventional studies evaluating its impact on functional recovery during stroke rehabilitation. This study aimed to assess whether daily vitamin D3 supplementation enhances functional recovery. 

Methods: 

 This prospective, randomized, placebo-controlled, single-blind study included 159 patients (mean age: 62.5 ± 8.4 years) with a first ischemic stroke that were admitted for early rehabilitation. The participants were randomly allocated to receive 2000 IU of vitamin D3 daily (n = 79) or a placebo (n = 80) for six weeks. The functional outcomes were measured using the Barthel index (BI) and modified Rankin scale (mRS) at baseline and after 42 days. The serum 25-hydroxyvitamin D [25(OH)D] and insulin-like growth factor 1 (IGF-1) levels were analyzed. 

Results: 

Vitamin D3 supplementation significantly increased the serum 25(OH)D levels (p < 0.001). Supplementation was associated with improved BI scores (β = 0.07, p = 0.006). A higher BMI (β = −0.06, p = 0.033), higher NIHSS scores (β = −0.18, p = 0.036), hypertension, and statin use negatively impacted functional recovery. Anticoagulant use was correlated with higher mRS scores, indicating greater disability (p = 0.04). 

Conclusions: 

 Vitamin D3 supplementation positively influences the functional outcomes during post-stroke rehabilitation, supporting its potential role in enhancing neuroplasticity and recovery. Larger multi-center trials are needed to confirm these findings and optimize vitamin D supplementation strategies.

Keywords:

ischemic stroke; vitamin D3 supplementation; rehabilitation; Barthel index; modified Rankin scale; neuroplasticity; randomized controlled trial

1. Introduction

Every year, millions of people worldwide experience a stroke, regardless of race, origin, or socioeconomic status [1]. Cerebrovascular diseases, including strokes, rank as the second leading cause of death globally [2]. The full recovery of function and perception occurs in only 10% of patients. Approximately 15% of stroke patients die in the early phase, while 25% experience a recurrent stroke. The risk of recurrence is highest within the first and second years following the initial event. Individuals who have experienced a stroke are at a significantly greater risk of a second stroke compared to their peers of the same age and sex who have not had a stroke [3]. Stroke prevention strategies focus primarily on behavioral and lifestyle factors [4]. Hence, managing risk factors plays a crucial role in medical care. Strokes are the leading cause of disability in individuals over the age of 45 [5].

Stroke timing critically influences the potential for neuroplasticity and functional recovery, particularly during the early phase of rehabilitation. Indeed, recent findings underscore the importance of initiating therapy promptly to leverage optimal brain reorganization [6]. It is generally accepted that cortical reorganization peaks 7–14 days post-stroke and persists for approximately one month [7]. Early rehabilitation reduces disability at the end of the rehabilitation period, lowering future healthcare costs. Global concerns about vitamin D deficiencies are increasing, affecting nearly half of the population worldwide [8,9].

A vitamin D deficiency is now recognized as a public health issue. Recent population-based studies indicate that low vitamin D levels predict future strokes. Poland, characterized by limited sunlight exposure, is among the countries where vitamin D deficiencies are prevalent [10,11]. Low serum 25-hydroxyvitamin D (25[OH]D) levels are linked to cardiovascular, musculoskeletal, infectious, autoimmune, and malignant diseases [12]. Vitamin D has been shown to have neuroprotective, neuromuscular, and osteoprotective properties, potentially reducing cognitive and functional impairments in post-stroke patients [13]. The current literature suggests that vitamin D supplementation and neuroprotective diets can enhance the efficacy of stroke rehabilitation and recovery.

Vitamin D is believed to support neurological function and recovery through several interconnected pathways. First, vitamin D receptors (VDRs) are expressed in various regions of the central nervous system, including the cortex and hippocampus, suggesting that vitamin D can exert both genomic and non-genomic effects on neuronal survival and plasticity [14,15]. In the setting of an ischemic stroke, vitamin D may mitigate neuroinflammation by downregulating pro-inflammatory mediators such as interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α), potentially limiting secondary neuronal damage [16,17]. Furthermore, vitamin D has been shown to influence the expression of neurotrophic factors—such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF)—which are crucial for neuronal repair and synaptic plasticity [18]. Additional research also points to an improvement in endothelial function and microcirculatory blood flow under optimal vitamin D levels, contributing to reduced ischemic injury in the affected brain tissue [19]. Collectively, these mechanisms support the hypothesis that an adequate vitamin D status may facilitate improved functional recovery and neurorehabilitation outcomes in post-stroke patients.

However, interventional studies remain scarce, highlighting the urgent need for randomized controlled trials (RCTs) to evaluate the impact of vitamin D supplementation on stroke outcomes [20]. Therefore, this study aimed to determine whether vitamin D3 supplementation influences the functional recovery in patients undergoing a 6-week neurological rehabilitation program during the regenerative–compensatory phase.

More at link.

Combination therapy with vitamin D3, progesterone, omega-3 fatty acids and glutamine reverses coma and improves clinical outcomes in patients with severe traumatic brain injuries: A case series

You can ask your doctors if anything here would help in stroke recovery. Doesn't know, then the correct and only answer is for them to contact researchers to get an answer.  Not doing anything, call the president and ask what the fuck is the responsibility of the stroke doctors. Delivering the status quo of stroke rehab means that the stroke president also needs to be fired.  Or you could look up these:

• progesterone (11)
• omega-3 (77)
• vitamin D3 (5)
• glutamine (2)

Combination therapy with vitamin D3, progesterone, omega-3 fatty acids and glutamine reverses coma and improves clinical outcomes in patients with severe traumatic brain injuries: A case series

How to cite this article:

Matthews LR, Danner OK, Ahmed YA, Dennis-Griggs DM, Frederick A, Clark C, Moore R, DuMornay W, Childs EW, Wilson KL. Combination therapy with vitamin d3, progesterone, omega 3-fatty acids and glutamine reverses coma and improves clinical outcomes in patients with severe traumatic brain injuries: A case series. International Journal of Case Reports and Images 2012;4(3):143–149.

Abstract

Introduction: Traumatic brain injury (TBI) is a major public health problem and a leading cause of death and disability in the United States. Management of patients with TBI has changed very little over the last 20 years. Case Series: A case series of three patients with severe TBIs who were aggressively treated with vitamin D3, progesterone, omega 3-fatty acids, and enteral glutamine for six weeks, termed neuroceutical augmentation for traumatic brain injury (NATBI), with very favorable outcomes. Conclusion: A large clinical study trial using these four supplements (NATBI) together is warranted.

Keywords: Traumatic brain injury, Vitamin D3, Omega-3 fatty acids, Loveza, Progesterone, Cerebral edema, Glutamine

Introduction

Traumatic brain injury (TBI) is a major public health problem. According to CDC it affects over 1.7 million people annually in U.S. with 275,000 hospitalizations and 52,000 deaths. [1] The medical cost for treating TBI patients in the United States in 2010 was $76.5 billion and rising annually. [1] Primary causes for TBI include the following: motor vehicle crashes, falls, assaults and sports or recreation-related injuries (concussions). Finding the right treatment to reduce mortality rates and improve the clinical outcomes in TBI patients has been elusive. Management of patients with TBI has changed very little over the last 20 years. Advancements in the treatment of TBI requires great understanding of the biochemical mechanisms of the brain during a normal resting state as well as the metabolism after a severe traumatic event. Brain metabolism is markedly altered during TBI. After the initial insult to the brain, the brain's metabolism is altered and can increase up to 140% of its normal metabolism. Vitamin D (a steroid hormone) and omega-3 fatty acids (an essential fatty acid) are both very powerful anti-inflammatory agents that reduce cerebral edema and swelling. Glutamine becomes an essential amino acid during stress and produces the extra glucose (via the Cori cycle) that is used by the injured brain and the extra glucose used by the immune response system to fight off infection during stress. Progesterone (also a steroid hormone) is a neuroprotector of injured brain cells and potentiates the effect of vitamin D. These agents are all immune modulators which work synergistically to prevent secondary brain injury by limiting or decreasing inflammation; an increasing well-recognized cause of ongoing brain swelling after a primary injury. They are also neuroprotectors that makes the neurons more resistant to stress, ischemia, hypothermia, hyperthermia, hypoglycemia, hyperglycemia, hypotension, and hypertension. Immune modulation with nutritional supplements is a rapidly advancing field with a very promising future in treating TBI as well as other critically injured/ill patients. We present a case series of three patients with severe TBIs who were aggressively treated with vitamin D3, progesterone, omega-3 fatty acids and enteral glutamine for up to six weeks, termed neuroceutical augmentation for traumatic brain injury (NATBI), with very favorable outcomes. [2] [3] [4] [5] Patients in a coma with severe TBI (Glascow Coma Score <8) who were admitted to a Level I trauma center were evaluated in a prospective observational study. Patients were treated with a neuroceutical combination of vitamin D3, omega-3 fatty acids, progesterone, and glutamine initially via a nasogastric tube and later orally for six weeks. Primary outcomes were mortality rate and return to recovery which was defined as a Glascow Coma Score (GCS) of 10 or greater.NATBI protocol works on multiple levels and neuroprotective pathways in TBI patients by down regulating cytokine production, preventing oxidative stress (free radical oxygen formation), decreasing cerebral edema, and inflammation, thus limiting secondary brain injury in contradistinction to progesterone therapy alone (Protect III study). [3] [4] [5] In addition, our NATBI regimen is relatively inexpensive, safe, and very effective at reducing brain and systemic inflammation post-injury.

Leslie R Matthews1, Omar K Danner1, Y A Ahmed2, Diane M Dennis-Griggs1, Alexis Frederick1, Clarence Clark1, Ronald Moore1, Wilson DuMornay1, Ed W Childs1, Kenneth L Wilson1

1Morehouse School of Medicine, Department of Surgery, 720 Westview Drive, SW, Atlanta, GA, USA. 2Department of Epidemiology, King Saud University, College of Pharmacy, Riyadh, Kingdom of Saudia of Arabia.

doi:10.5348/ijcri-2013-03-281-CS-2 Address correspondence to: Leslie Ray Matthews MD, FACS, 720 Westview Drive SW, Atlanta Georgia 30228 USA Phone: (404) 6162391 Fax: (404) 6161417 Email: lematthews@msm.edu Access full text article on other devices Access PDF of article on other devices

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Association between vitamin D status and cognitive impairment in acute ischemic stroke patients: a prospective cohort study

I see nothing here that suggests that this is being written up as a stroke protocol and distributed worldwide to all stroke hospitals and doctors. Isn't that the minimum needed to 'do no harm'? 

Is this just Vitamin D or D3? Inquiring minds want to know.  Does low vitamin D cause this problem or the underlying reason that initially caused the low levels the real problem? Have you actually identified the root cause?

Vitamin D3 Could Help Prevent, Repair Cardiovascular System Damage

The latest here:

Association between vitamin D status and cognitive impairment in acute ischemic stroke patients: a prospective cohort study

Authors Chen H, Liu Y, Huang G, Zhu J, Feng W, He J
Received 11 September 2018
Accepted for publication 18 November 2018
Published 10 December 2018 Volume 2018:13 Pages 2503—2509
DOI https://doi.org/10.2147/CIA.S187142
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 3
Editor who approved publication: Dr Wu

Huijun Chen,^1,* Yuntao Liu,^1,* Guiqian Huang,^1,* Jie Zhu,² Wenqian Feng,² Jincai He<sup>1

1</sup>Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China; ²Department of Mental Health, Mental Health School, Wenzhou Medical University, Wenzhou 325000, China

*These authors contributed equally to this work

Objective: Previous studies found that low vitamin D levels were modestly associated with risk of stroke and poor functional outcome after stroke. In addition, vitamin D deficiency has been linked with cognitive decline. Our study aimed to explore the potential relationship between vitamin D levels in the short-term acute phase of ischemic stroke and cognitive impairment at 1 month.
Methods: In total, 354 ischemic stroke patients were consecutively enrolled in the study and received 1-month follow-up. The serum levels of vitamin D were measured within 24 hours after admission. Cognitive function was evaluated by the Mini-Mental State Examination (MMSE) at 1 month after acute ischemic stroke. Cognitive impairment was defined according to different education levels.
Results: According to MMSE scores, 114 participants (32.2%) had cognitive impairment at 1 month. Patients with vitamin D deficiency were more likely to have cognitive impairment than those with vitamin D insufficiency and vitamin D sufficiency (P<0.001). After adjusting for potential confounders in our Cox proportional hazards model, vitamin D deficiency was independently associated with the development of cognitive impairment in acute ischemic stroke patients.
Conclusion: Independent of established risk factors, vitamin D deficiency in the short-term phase of ischemic stroke was associated with a higher incidence of 1-month cognitive impairment.

Keywords: vitamin D, cognitive impairment, ischemic stroke, Mini-Mental State Examination

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Vitamin D3 Could Help Prevent, Repair Cardiovascular System Damage

You can't do anything with this until your doctor gives you a protocol. Warning:

Is There Such a Thing As Too Much Vitamin D3?

The latest here:

Vitamin D3 Could Help Prevent, Repair Cardiovascular System Damage

Cholecalciferol, also known as vitamin D3, can significantly restore the damage to the cardiovascular system caused by several diseases, including hypertension, diabetes and atherosclerosis, according to new research from Ohio University.

Vitamin D3 may be effective in the treatment of hypertension and other cardiovascular diseases, including heart failure, myocardial infarction, vasculopathy, stroke and diabetes. Image credit: Aloísio Costa Latgé.

“Generally, vitamin D3 is associated with the bones. However, in recent years, in clinical settings people recognize that many patients who have a heart attack will have a deficiency of D3,” said Ohio University’s Professor Tadeusz Malinski.
“It doesn’t mean that the deficiency caused the heart attack, but it increased the risk of heart attack.”
“We use nanosensors to see why D3 can be beneficial, especially for the function and restoration of the cardiovascular system.”
Professor Malinski and his colleagues, Alamzeb Khan and Hazem Dawoud, have developed unique methods and systems of measurements using nanosensors to track the impacts of vitamin D3 on single endothelial cells, a vital regulatory component of the cardiovascular system.
A major discovery from these studies is that D3 is a powerful stimulator of nitric oxide, which is a major signaling molecule in the regulation of blood flow and the prevention of the formation of clots in the cardiovasculature. Additionally, D3 significantly reduced the level of oxidative stress in the cardiovascular system.
Most importantly, these studies show that treatment with D3 can significantly restore the damage to the cardiovascular system caused by several diseases, including hypertension, atherosclerosis, and diabetes, while also reducing the risk of heart attack.
“There are not many, if any, known systems which can be used to restore cardiovascular endothelial cells which are already damaged, and D3 can do it,” Professor Malinski said.
“This is a very inexpensive solution to repair the cardiovascular system. We don’t have to develop a new drug. We already have it.”
These studies are the first to identify the molecular mechanism of vitamin D3-triggered restoration of the function of damaged endothelium in the cardiovasculature.
While the studies were performed using a cellular model of hypertension, the implication of D3 on dysfunctional endothelium is much broader.
The dysfunction of endothelium is a common denominator of several cardiovascular diseases, particularly those associated with ischemic events.
“Therefore, D3 may be of clinical importance in the restoration of dysfunctional cardiac endothelium after heart attack, capillary endothelium after brain ischemia (stroke), hypovolemia, vasculopathy, diabetes and atherosclerosis,” the researchers said.
The results are published in the International Journal of Nanomedicine.
_____
Alamzeb Khan et al. 2018. Nanomedical studies of the restoration of nitric oxide/peroxynitrite balance in dysfunctional endothelium by 1,25-dihydroxy vitamin D3 — clinical implications for cardiovascular diseases. International Journal of Nanomedicine 13: 455-466; doi: 10.2147/IJN.S152822

Study Shows Vitamin D3 Could Help Heal or Prevent Cardiovascular Damage

You'll have to ask your doctor whether this refers to the brain also using the old definition of cardiovascular or not. Your doctors knowledge of even understanding the question tells you a tiny bit of how up-to-date s/he is.  Does your doctor have enough brains to be able extrapolate this to brain vasculature also without clinical studies? Do not do on your own you could overdose without enough knowledge. .
6 Side Effects of Too Much Vitamin D - Healthline

The latest here:
Study Shows Vitamin D3 Could Help Heal or Prevent Cardiovascular Damage

A new study conducted by Ohio University scientists suggests that a little more sunlight might help restore damage to your cardiovascular system.

The study shows that Vitamin D3 - which is made by the body naturally when skin is exposed to the sun - can significantly restore the damage to the cardiovascular system caused by several diseases, including hypertension, diabetes and atherosclerosis. Vitamin D3 supplements are also available over-the-counter.

The study, by Marvin and Ann Dilley White Chair and Distinguished Professor Dr. Tadeusz Malinski and two graduate students, Alamzeb Khan and Hazem Dawoud, has been published in the International Journal of Nanomedicine.

"Generally, Vitamin D3 is associated with the bones. However, in recent years, in clinical settings people recognize that many patients who have a heart attack will have a deficiency of D3. It doesn't mean that the deficiency caused the heart attack, but it increased the risk of heart attack," Malinski said. "We use nanosensors to see why Vitamin D3 can be beneficial, especially for the function and restoration of the cardiovascular system."

Malinski's team has developed unique methods and systems of measurements using nanosensors, which are about 1,000 times smaller in diameter than a human hair, to track the impacts of Vitamin D3 on single endothelial cells, a vital regulatory component of the cardiovascular system. A major discovery from these studies is that vitamin D3 is a powerful stimulator of nitric oxide (NO), which is a major signaling molecule in the regulation of blood flow and the prevention of the formation of clots in the cardiovasculature. Additionally, vitamin D3 significantly reduced the level of oxidative stress in the cardiovascular system.

Most importantly, these studies show that treatment with vitamin D3 can significantly restore the damage to the cardiovascular system caused by several diseases, including hypertension, atherosclerosis, and diabetes, while also reducing the risk of heart attack. These studies, performed on cells from Caucasian Americans and African Americans, yielded similar results for both ethnic groups.

"There are not many, if any, known systems which can be used to restore cardiovascular endothelial cells which are already damaged, and Vitamin D3 can do it," Malinski said. "This is a very inexpensive solution to repair the cardiovascular system. We don't have to develop a new drug. We already have it."

These studies, performed at Ohio University, are the first to identify the molecular mechanism of vitamin D3-triggered restoration of the function of damaged endothelium in the cardiovasculature. While these studies were performed using a cellular model of hypertension, the implication of vitamin D3 on dysfunctional endothelium is much broader. The dysfunction of endothelium is a common denominator of several cardiovascular diseases, particularly those associated with ischemic events.

Therefore, the authors suggest that vitamin D3 may be of clinical importance in the restoration of dysfunctional cardiac endothelium after heart attack, capillary endothelium after brain ischemia (stroke), hypovolemia, vasculopathy, diabetes and atherosclerosis. This suggestion is strongly supported by several clinical studies which indicate that vitamin D3 at doses higher than those currently used for the treatment of bone diseases, may be highly beneficial for the treatment of the dysfunctional cardiovascular system.

"Professor Malinksi has an international reputation for outstanding and innovative research related to the cardiovascular system," Ohio University Dean of Arts and Sciences Robert Frank said. "This latest work is yet another example of his impact on this field."

Study: Taking high dose of vitamin D3 safe for people with multiple sclerosis

Well, well. You can have your doctor resolve the two different research results. Sometimes I wonder if researchers read other research in their areas of expertise. Or are patients expected to catch these competing results?

Monthly High-Dose Vitamin D Treatment for the Prevention of Functional Decline but causing falls

The latest here:

Study: Taking high dose of vitamin D3 safe for people with multiple sclerosis

Taking a high dose of vitamin D3 is safe for people with multiple sclerosis and may help regulate the body's hyperactive immune response, according to a pilot study published by Johns Hopkins physicians in the Dec. 30 online issue of Neurology, the medical journal of the American Academy of Neurology.
"These results are exciting, as vitamin D has the potential to be an inexpensive, safe and convenient treatment for people with MS," says study author Peter Calabresi, M.D., director of the Johns Hopkins Multiple Sclerosis Center and professor neurology at the Johns Hopkins University School of Medicine. "More research is needed to confirm these findings with larger groups of people and to help us understand the mechanisms for these effects, but the results are promising."
Low levels of vitamin D in the blood are tied to an increased risk of developing MS. People who have MS and low levels of vitamin D are more likely to have greater disability and more disease activity.

For the study, 40 people with relapsing-remitting MS received either 10,400 international units or 800 international units of vitamin D3 supplements per day for six months. Patients with severe vitamin D deficiency were not included in the study. The current recommended daily allowance of vitamin D3 is 600 international units. Blood tests at the start of the study and again at three and six months measured the amount of vitamin D in the blood and the response in the immune system's T cells, which play a key role in MS.
While researchers are still determining the optimal level of vitamin D in the blood for people with MS, a suggested range of 40 to 60 nanograms per milliliter (ng/ml) has been proposed as a target. Participants taking the high dose of vitamin D reached levels within the proposed target, whereas the group taking the low dose did not reach the target.
Side effects from the vitamin supplements were minor and were not different between the people taking the high dose and the people taking the low dose. One person in each group relapsed.
The people taking the high dose had a reduction in the percentage of inflammatory T cells related to MS severity, specifically IL-17+CD4+ and CD161+CD4+ cells. When the increase in vitamin D levels in the blood over base line levels was greater than 18 ng/ml, every additional 5 ng/ml increase in vitamin D led to a 1 percent decrease in the percentage of IL-17+CD4+ T cells in the blood. The people taking the low dose did not have any noticeable changes in the percentages of their T cell subsets.
"We hope that these changes in inflammatory T cell responses translate to a reduced severity of disease," says Calabresi. "Other clinical trials are underway to determine if that is the case."

Source:

Johns Hopkins Medicine

Cholecalciferol (Vitamin D3) Improves Myelination and Recovery after Nerve Injury

This is a straight up question to your doctor. Did your stroke cause damage to the myelin sheaths in your white matter? What protocol is your doctor using to recover that loss?

Cholecalciferol (Vitamin D3) Improves Myelination and Recovery after Nerve Injury

Abstract

Previously, we demonstrated i) that ergocalciferol (vitamin D₂) increases axon diameter and potentiates nerve regeneration in a rat model of transected peripheral nerve and ii) that cholecalciferol (vitamin D3) improves breathing and hyper-reflexia in a rat model of paraplegia. However, before bringing this molecule to the clinic, it was of prime importance i) to assess which form – ergocalciferol versus cholecalciferol – and which dose were the most efficient and ii) to identify the molecular pathways activated by this pleiotropic molecule. The rat left peroneal nerve was cut out on a length of 10 mm and autografted in an inverted position. Animals were treated with either cholecalciferol or ergocalciferol, at the dose of 100 or 500 IU/kg/day, or excipient (Vehicle), and compared to unlesioned rats (Control). Functional recovery of hindlimb was measured weekly, during 12 weeks, using the peroneal functional index. Ventilatory, motor and sensitive responses of the regenerated axons were recorded and histological analysis was performed. In parallel, to identify the genes regulated by vitamin D in dorsal root ganglia and/or Schwann cells, we performed an in vitro transcriptome study. We observed that cholecalciferol is more efficient than ergocalciferol and, when delivered at a high dose (500 IU/kg/day), cholecalciferol induces a significant locomotor and electrophysiological recovery. We also demonstrated that cholecalciferol increases i) the number of preserved or newly formed axons in the proximal end, ii) the mean axon diameter in the distal end, and iii) neurite myelination in both distal and proximal ends. Finally, we found a modified expression of several genes involved in axogenesis and myelination, after 24 hours of vitamin supplementation. Our study is the first to demonstrate that vitamin D acts on myelination via the activation of several myelin-associated genes. It paves the way for future randomised controlled clinical trials for peripheral nerve or spinal cord repair.