Vitamin D levels and related conditions
Discussion
Around 2011 I was really rough, off work for some 6 months and saw 8 different GPs at my practice until one finally suggested checking my vitamin D level. It came back at 12, when the recommended minimum was around 60 so I was put onto supplements. A year or so later I was diagnosed as T2 diabetic and have since been managing this via diet, exercise and medication with the nurse continually trying to push me to go onto insulin.
At one of my medication reviews some 10 years ago the GP removed the vitamin D supplement, but I have continued to buy them for myself and take 4000iu daily.
In parallel with this I have had issues with osteophytes (bone spurs) in my neck and, more recently, both shoulders. By chance yesterday I started looking to find out what the causes of osteophytes are; 2 main causes seem to be arthritis and vitamin D deficiency. Further to this I came across a significant link between vitamin D deficiency being a contributory factor towards T2 diabetes.
I’m obviously now going to get my vitamin D level checked but am beginning to think that this may be the cause of my health issues. I’d be interested in hearing if others have had similar experiences and whether, by increasing the vitamin D levels, you reversed the symptoms.
I’m not inclined to go back to my GP about this at the moment due to the lack of help that they’ve been in the past. Would this be an area for an endocrinologist to help with?
At one of my medication reviews some 10 years ago the GP removed the vitamin D supplement, but I have continued to buy them for myself and take 4000iu daily.
In parallel with this I have had issues with osteophytes (bone spurs) in my neck and, more recently, both shoulders. By chance yesterday I started looking to find out what the causes of osteophytes are; 2 main causes seem to be arthritis and vitamin D deficiency. Further to this I came across a significant link between vitamin D deficiency being a contributory factor towards T2 diabetes.
I’m obviously now going to get my vitamin D level checked but am beginning to think that this may be the cause of my health issues. I’d be interested in hearing if others have had similar experiences and whether, by increasing the vitamin D levels, you reversed the symptoms.
I’m not inclined to go back to my GP about this at the moment due to the lack of help that they’ve been in the past. Would this be an area for an endocrinologist to help with?
You might find it advantageous to introduce cod liver oil alongside your Vitamin D supplement intake. There's several products that combine the two.
I developed a pain where my spine joins my pelvis and in my shoulders. I knew exactly why - too heavy and too much sitting. I shed the weight and started exercising which helped but not totally. Started on the Omega 3 / Vit D supplements and seems to have cured the problem.
I developed a pain where my spine joins my pelvis and in my shoulders. I knew exactly why - too heavy and too much sitting. I shed the weight and started exercising which helped but not totally. Started on the Omega 3 / Vit D supplements and seems to have cured the problem.
CoolHands said:
But don’t you say in the first paragraph that you are and have been taking vitamin D? Also side note but is it D3 were meant to take as it can’t be made naturally? (Ie is d3 different from D?)
D3 alongside K2 in a similar quantity is the 'recommended' regime, I believe - something to do with the K2 ensuring calcium take-up in the desired places.Yes, no problems with my sense of smell. Not sure about the above point concerning calcium take up, as one of my issues is the growing of osteophytes around my neck and shoulders. When they reach a point that starts impinging on nerves then things get nasty. My neck problems took a couple of years to sort out - surgery was ruled out then due to the severity. Now I might be facing the knife because of them in my shoulders, hence why I'm keen to take all measures to prevent recurrence.
The k2 / calcification thing might be more cardiovascular? Could be worth asking your medical specialist about any potential linkages.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10351276/
Effects of vitamins K2 and D3 supplementation in patients with severe coronary artery calcification: a study protocol for a randomised controlled trial
https://pmc.ncbi.nlm.nih.gov/articles/PMC10351276/
Effects of vitamins K2 and D3 supplementation in patients with severe coronary artery calcification: a study protocol for a randomised controlled trial
paper said:
Vitamin K and the calcification process
The most familiar K vitamin is phylloquinone (vitamin K1), as it is essential for the activation of several coagulation factors. Menaquinone-7 (MK-7), also known as vitamin K2, is another very important vitamin K species with mostly extra-hepatic effects due to higher concentrations outside the liver. Even though some pathways are shared, vitamin K2 is thought to be the primary activator of non-hepatic proteins related to the inhibition of arterial calcification, that is, matrix-Gla proteins (MGP).5–8 The activation of these important proteins is, however, dependent on their synthesis, which again is stimulated by vitamin D3.9 Without both synthesis and activation of relevant proteins, the balance of cellular calcium uptake and the mineralisation process in bone and blood vessels is impaired. The inhibiting effect of the vitamin K-dependent proteins on calcification was originally showed by Luo et al in 1997.10 In a mice model, they found activated (carboxylated) MGP to be an important inhibitor of vascular calcification. More recent randomised clinical trials have tested this theory with vitamin K2 supplementation in different populations finding only a discreet reduction in CAC.11 12 Contrarily, observational studies suggest that long-term use of vitamin K antagonists is associated with increased vascular calcification.13–16 Furthermore, combined low vitamins K and D status has been associated with increased all-cause mortality risk compared with adequate vitamins K and D status.17 A synergistic effect of the two vitamins on bone and cardiovascular health has been suggested.18 Currently, no recommendations of vitamin K2 supplementation are available. As demonstrated in a randomised controlled trial, there is a dose-dependent decrease of uncarboxylated MGP concentrations by vitamin K2 supplementation (180 µg/day, 360 µg/day or placebo).19 Thus, we know that the daily intake in the Western world is not sufficient to meet the request for a complete activation of MGP. Additionally, there is no documented toxicity for vitamin K1 or vitamin K2, and the WHO has set no upper tolerance level for vitamin K intake.20
The effect of supplementation with high-dose vitamin K2 (720 µg/day) and vitamin D (25 µg/day) over 2 years was examined in the very recent Danish AVADEC (Aortic Valve DECalcification) Trial.21 Aortic valve calcification progression was non-significantly decreased.22 However, the supplementation appeared to slow down the progression of CAC, especially in patients with severe CAC (score>400). It also reduced progression of the non-calcified coronary plaque volume. Very importantly, the total number of cardiac events and all-cause death was significantly lower (unpublished data). As these findings were secondary outcomes, the results are only hypothesis generating and a confirmatory trial is requested.
The most familiar K vitamin is phylloquinone (vitamin K1), as it is essential for the activation of several coagulation factors. Menaquinone-7 (MK-7), also known as vitamin K2, is another very important vitamin K species with mostly extra-hepatic effects due to higher concentrations outside the liver. Even though some pathways are shared, vitamin K2 is thought to be the primary activator of non-hepatic proteins related to the inhibition of arterial calcification, that is, matrix-Gla proteins (MGP).5–8 The activation of these important proteins is, however, dependent on their synthesis, which again is stimulated by vitamin D3.9 Without both synthesis and activation of relevant proteins, the balance of cellular calcium uptake and the mineralisation process in bone and blood vessels is impaired. The inhibiting effect of the vitamin K-dependent proteins on calcification was originally showed by Luo et al in 1997.10 In a mice model, they found activated (carboxylated) MGP to be an important inhibitor of vascular calcification. More recent randomised clinical trials have tested this theory with vitamin K2 supplementation in different populations finding only a discreet reduction in CAC.11 12 Contrarily, observational studies suggest that long-term use of vitamin K antagonists is associated with increased vascular calcification.13–16 Furthermore, combined low vitamins K and D status has been associated with increased all-cause mortality risk compared with adequate vitamins K and D status.17 A synergistic effect of the two vitamins on bone and cardiovascular health has been suggested.18 Currently, no recommendations of vitamin K2 supplementation are available. As demonstrated in a randomised controlled trial, there is a dose-dependent decrease of uncarboxylated MGP concentrations by vitamin K2 supplementation (180 µg/day, 360 µg/day or placebo).19 Thus, we know that the daily intake in the Western world is not sufficient to meet the request for a complete activation of MGP. Additionally, there is no documented toxicity for vitamin K1 or vitamin K2, and the WHO has set no upper tolerance level for vitamin K intake.20
The effect of supplementation with high-dose vitamin K2 (720 µg/day) and vitamin D (25 µg/day) over 2 years was examined in the very recent Danish AVADEC (Aortic Valve DECalcification) Trial.21 Aortic valve calcification progression was non-significantly decreased.22 However, the supplementation appeared to slow down the progression of CAC, especially in patients with severe CAC (score>400). It also reduced progression of the non-calcified coronary plaque volume. Very importantly, the total number of cardiac events and all-cause death was significantly lower (unpublished data). As these findings were secondary outcomes, the results are only hypothesis generating and a confirmatory trial is requested.
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