From Aging and calcium as an environmental factor. (emphasis mine)
"The consequences of calcium deficiency might thus include not only osteoporosis, but also arteriosclerosis and hypertension due to the increase of calcium in the vascular wall, amyotrophic lateral sclerosis and senile dementia due to calcium deposition in the central nervous system, and a decrease in cellular function, because of blunting of the difference in extracellular-intracellular calcium, leading to diabetes
mellitus, immune deficiency and others.
I highlighted amyotrophic lateral sclerosis in red, as many Facebook friends have been having buckets of water & ice cubes tipped over themselves to raise money for research into this horrible & ultimately fatal condition.
So, what prevents & reverses migration of calcium from hard tissues to soft tissues?
Clue: It carboxylates osteocalcin in bone matrix Gla proteins. Yes, it's Vitamin K2.
Before I start on what may be the most important thing that I've ever written, here's Don't Stop Movin' by S Club 7. It's a clue to what's coming.
The problem:
Insulin Resistance (IR) is a major problem for a significant percentage of the population in the developed world. If left untreated, it can deteriorate into Type 2 Diabetes (T2D). See Type 2 diabetes in the UK.
IR & T2D can cause:-
High fasting & postprandial serum glucose, which increases the risk factor for Coronary Heart Disease, Retinopathy, Neuropathy& Nephropathy (Kidney failure), amongst other things. High fasting & postprandial serum triglycerides, which increases the risk factor for Coronary Heart Disease. See Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity. High serum cholesterol, which increases the risk factor for Coronary Heart Disease. High serum Free Fatty Acids (a.k.a. FFAs a.k.a. NEFAs) from IR fat cells, which increases the risk factor for Sudden cardiac death and also worsens IR in liver & muscle cells. High serum uric acid, which increases the risk factor for Gout & Uric acid Kidney stones. Hypertension, which raises the risk factor for Coronary Heart Disease, Strokes & Kidney failure. Excessive appetite after eating high-GL carbohydrates, leading to overeating & obesity. Lethargy/sleepiness after eating almost anything, but especially after eating high-GL carbohydrates, due to postprandial hyperinsulinaemia.
Possible causes (IR is multi-factorial) and solutions:
1."Bad" genes. My genes aren't particularly good, but it is possible to change the expression of genes. See below.
2.Full cells. A full cell is an IR cell. Consider Liver, Muscle and Fat cells:-
a) Liver cells: Liver cells are a 2-way street. "Stuff" (e.g. FFAs, Glucose & Fructose) goes in and "stuff" (e.g. Ketones & Glucose) comes out. Glucose normally comes out of the liver at a rate of ~5g/hour to fuel the brain, but this can increase a lot under the control of Insulin, Glucagon & Cortisol. If more stuff goes in than comes out, liver glycogen stores fill up and vice-versa. When liver glycogen stores become full, liver cells down-regulate processes that produce liver glycogen e.g. hexokinase & Glu-T2 transporters. Liver cells effectively become IR, to stop more stuff from going in.
However, fructose is transported by Glu-T5 transporters which are insulin-independent & taken up by fructokinase which has a high affinity for fructose, so fructose effectively "barges its way in" to the liver. This is why fructose is a problem for people who have permanently full liver glycogen stores.
b) Muscle cells: Muscle cells are a 1-way street as far as Glucose is concerned, though Amino Acids can go in & come out. Muscle glycogen cannot be used to produce blood glucose - it can only be used by muscles. When muscle glycogen stores become full, muscle cells down-regulate processes that produce muscle glycogen e.g. hexokinase & Glu-T4 transporters. Muscle cells effectively become IR to stop more stuff from going in.
As per It's all in a day's work (as measured in Joules), muscle cells use mostly fat at rest & lowish-intensity exercise. Glycogen usage increases rapidly as exercise intensity increases. Now do you see the significance of the music video above? Intense exercise (e.g. Running, Sprinting, Resistance training with weights, parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your muscle cells and makes them Insulin Sensitive.
c) Fat cells: Fat cells are a 2-way street. Fat cells are a bit like balloons that are full of holes. As stuff (e.g. FFAs & glucose) goes in, the balloon expands to accommodate it. As more stuff goes in and the balloon gets bigger, the internal pressure increases and the holes get bigger, so stuff (e.g. FFAs & glycerol) comes out at a faster rate. At some level of fullness, stuff comes out as fast as it goes in. At that point, fat cells are effectively IR. So, don't overstuff your fat cells by getting too fat. If you are already too fat, medium intensity exercise (e.g. Walking, Power Walking, Jogging, "Aerobics", parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your fat cells and makes them Insulin Sensitive.
3. Empty (of glycogen) cells.
If carbohydrate intake is too low (say, less than 50g/day), physiological Insulin Resistance develops in order to spare glucose for the brain (as parts of the brain run on glucose only) and red blood cells. This is reversible on increasing carbohydrate intake. People who are on ketogenic diets are advised to increase their carbohydrate intake for a few days prior to taking an Oral Glucose Tolerance Test. See HIGH CARBOHYDRATE DIETS AND INSULIN EFFICIENCY.
In January 2003, I had Impaired Glucose Tolerance/Metabolic Syndrome/Prediabetes (fasting serum glucose = 5.8mmol/L & 2 hours post-75g glucose load serum glucose = 8.7mmol/L). A sandwich used to send me to sleep.
By September 2008, I had Normal Glucose Tolerance (fasting serum glucose
= 5.0mmol/L & 2 hours post-75g glucose load serum glucose =
3.7mmol/L). I also no longer suffered from carbohydrate-induced comas. I was also about the same weight that I was in 2003, so the improvement wasn't due to weight loss. Hypovitaminosis D was the primary contributor to my IR.
So, either use a UVB sun-lamp as per instructions to receive a sub-erythemal dose (not quite going pink) or get tested by your GP and supplement with Vitamin D3 accordingly. I take 5,000iu of Vitamin D3/day.
5.Deficiency in Magnesium.
See Magnesium and type 2 diabetes. For the top 999 foods highest in Magnesium per 200kcal serving, see HERE. I've been taking ~4g of Epsom Salts/day (~400mg Mg/day, dissolved in 2 litres of fluids that I drink each day, to avoid laxative effects) since 2003 as it reversed osteoporosis in my lumbar spine.
10.Excessive intake of man-made trans-fats.
Base your diet on minimally refined produce rather than over-refined &/or moreish food products.
11.Excessive intake of chemicals.
Don't swallow toothpaste (fluoride) or disclosing tablets (as they may contain iodine). Don't hold till receipts between your lips (may be coated in BPA).
Finally, the obligatory picture. Hannah Spearritt is rather nice. :-p
I nearly forgot! Today, when I arrived at mum's nursing home, I found her reading a book. She hasn't done that for over a year. She even knew that it was Wednesday. Ketogenic diet for the win. Mum now has a dual-fuel brain. EDIT: Mum passed away in April 2013, so although it's possible to slow the progression of Lewy Body Dementia and reduce the symptoms of it, it wasn't possible to cure it.
Vitamin D is known as the "Sunshine Vitamin" and it was once thought that a deficiency in it was rare and that it was only involved in calcium homoeostasis in bones and that a lack of it caused only Rickets. Recent research has shown that not only is Vitamin D involved in a whole host of bodily processes, but also that an insufficiency in it is very common, leading to an increased risk factor for a whole host of degenerative diseases, such as Coronary Heart Disease and Cancer.
According to Hyppönen and Power, in a large sample of the white British population born in 1958, 60.9% of subjects had serum 25(OH)D (the active metabolite of Vitamin D) of less than 75nmol/L in Summer & Autumn, and 87.1% had serum 25(OH)D of less than 75nmol/L in Winter & Spring. To convert units from nmol/L to ng/mL, divide by 2.5.
Here's my experience of Vitamin D3. For many years, I was struggling to cope with my job and I eventually took early retirement on the grounds of ill-health. In mid-2006 I was given a serum 25(OH)D test and the result was 73nmol/L. As the Reference Range for serum 25(OH)D is 50-200 nmol/L, I was technically not deficient in Vitamin D. Subsequent events suggested otherwise.
In January 2007, after reading the above study and a study by Vieth, Kimball, Hu and Walfish, I began to supplement with 2,000iu/day of Vitamin D3 and also used a UVB+IR lamp for 3 minutes each night. At first, nothing happened and I was pretty sceptical about getting any improvement. However, after about 8 weeks, I began to notice an awakening in my brain. This continued, and by March 2007, I was feeling quite perky. Friends commented on the fact that I had become very chatty and I was also waking early in the morning raring to go, totally unlike my former self. In May 2007, I had another serum 25(OH)D test and the result was 115nmol/L. Another interesting result was my serum triglycerides, something that's usually always higher than desirable. My TGs were 1.4mmol/L (RR less than 1.8mmol/L). This was the lowest result since tests began in 2002.
I began to get bored with standing around stark naked in front of a UV lamp for 3 minutes each night and I stopped doing this. Slowly, my brain began to go back to sleep. I couldn't understand why as I thought that 2,000iu/day of Vitamin D3 (5 x RDA) was more than enough.
In November 2007, I had another serum 25(OH)D test. When I saw my endocrinologist in December 2007, I was quite shocked to see that the result was now 70nmol/L. I immediately increased my Vitamin D3 intake to 5,000iu/day (12.5 x RDA) and within 2 weeks, my brain started to wake up again. In May 2008, serum 25(OH)D was 173nmol/L and in September 2008 it was 163nmol/L. I'm still taking 5,000iu/day.
For a list of the foods highest in Vitamin D, see here. Beware of foods that have been supplemented, as Vitamin D2 may have been used. This is less effective than Vitamin D3 according to Armas, Hollis and Heaney. Vegetarians and vegans may not want to eat foods containing Vitamin D3 as this is sourced from animals (e.g. the lanolin from a sheep's coat). Eating the Standard English Diet, it is difficult to obtain 5,000iu/day of Vitamin D. The cheapest way to get a lot of it is by going out in the sun in a swimsuit for 20 or so minutes in the middle of the day in Summer and Autumn, which costs absolutely nothing. As Vitamin D is fat-soluble, the body can build up stores to keep itself supplied during Winter and Spring.
Vitamin D deficiency, Insulin Resistance and The Metabolic Syndrome and Type 2 Diabetes
According to Hyppönen and Power, there is a strong association between decreasing 25(OH)D, increasing Body Mass Index (BMI) and increasing HbA1c (glycated haemoglobin).
According to Chiu, Chu, Go and Saad, there is a positive correlation of 25(OH)D concentration with insulin sensitivity and a negative effect of hypovitaminosis D on ß cell function. Subjects with hypovitaminosis D are at higher Relative Risk of Insulin Resistance and The Metabolic Syndrome.
In January 2003, I had Impaired Glucose Tolerance (fasting serum glucose =
6.0mmol/L and 2 hours post-75g glucose load serum glucose = 8.7mmol/L). A sandwich used to send me to sleep.
By September 2008, I had Normal Glucose Tolerance (fasting serum glucose = 5.0mmol/L and 2 hours post-75g glucose load serum glucose = 3.7mmol/L). I also no longer suffered from hyperinsulinaemic sleeps. Result!
Vitamin D deficiency and Cancer
According to Lappe, Travers-Gustafson, Davies, Recker and Heaney, subjects receiving 1400-1500mg/day supplemental calcium and 1100iu/day supplemental Vitamin D3 have a Relative Risk of getting any type of cancer of 0.402 which is equivalent to a 60% reduction in the risk of getting cancer compared to the non-supplementing group.
If the first 12 months results are discarded (to exclude any subjects who already had cancer when they started the study), the RR is 0.232 which is equivalent to a 77% reduction in the risk of getting cancer. I wonder what the result would have been had 5,000iu/day of Vitamin D3 been used.
See also Diaz, Paraskeva, Thomas, Binderup and Hague.
Vitamin D deficiency and Mental function
According to Vieth, Kimball, Hu and Walfish as mentioned above, supplementing with 4,000iu/day of Vitamin D3 produces a large reduction in the "Miserableness Factor" without affecting serum Calcium levels.
According to Gloth, Alam and Hollis, Improvement in 25(OH) D is significantly associated with improvement in depression scale scores in a group of 15 subjects with SAD.
According to Cherniack, Troen, Florez, Roos and Levis, Hypovitaminosis D is prevalent among older adults, and several studies suggest an association between hypovitaminosis D and basic and executive cognitive functions, depression, bipolar disorder, and schizophrenia.
According to Dharmarajan, Akula, Kuppachi and Norkus, in the pilot study of older adults with gait imbalance and falls, vitamin D deficiency was observed in 54% of patients tested and previously unrecognised.
Vitamin D Deficiency and Chronic Pain
According to Plotnikoff and Quigley, all patients with persistent, non-specificmusculoskeletal pain are at high risk for the consequences of unrecognised and untreated severe hypovitaminosis D.
According to Al Faraj and Al Mutairi, Vitamin D deficiency is a major contributor to chronic low back pain in areas where vitamin D deficiency is endemic.
According to Gloth, Lindsay, Zelesnick and Greenough, there may be a pain syndrome associated with vitamin D depletion that appears as hyperaesthesia worsened by light, superficial pressure or even small increments of movement.
But doesn't the sun damage the skin and cause skin cancer?
Inappropriate sun exposure can certainly damage the skin.
Chronic overexposure to the sun (e.g. farmers and other outdoor workers) causes wrinkly, leathery skin and skin cancers such as Basal Cell Carcinoma and Squamous Cell Carcinoma. These are benignskin cancers which are removable and rarely fatal.
Acute overexposure to the sun (e.g. people getting severe sunburn on foreign holidays) causes the much more serious Malignant Melanoma. This condition, if not caught early enough, has a very high risk of mortality.
It is possible to overdose with Vitamin D by supplementation. According to Vieth, published cases of vitamin D toxicity with hypercalcaemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intakes of greater than 40,000iu/day. See also Pharmacokinetics of vitamin D toxicity.
It isn't possible to overdose by sun exposure, as the metabolic processes down-regulate when ~10,000iu has been produced. To find out when the sun is strong enough to produce Vitamin D in your skin, see the Vitamin D Synthesis in Human Skin Calculator.
