By now, you've probably noticed that I'm a bit anti-statin. The "problem" with statins is that they reduce cholesterol synthesis in the liver by reducing the conversion of HydroxyMethylGlutaryl (HMG) Co-enzyme A (CoA) into Mevalonate by inhibiting the enzyme HMG CoA reductase.
Reducing Mevalonate reduces lots of other things e.g. Coenzyme Q10 synthesis, terpenoid synthesis, protein prenylation, cell membrane maintenance, hormones, protein anchoring, N-glycosylation and steroid biosynthesis which leads to cholesterol synthesis. Paradoxically, although cholesterol synthesis is reduced, Vitamin D level is increased. See also Atorvastatin increases 25-hydroxy vitamin D concentrations in patients with polycystic ovary syndrome.
Some of the above changes are undesirable in terms of all-cause mortality, so what would be ideal is a drug that just reduces serum cholesterol without doing anything else. Enter....Squalestatin a.k.a. Zaragozic Acid. This reduces the conversion of Farnesyl Pyrophosphate into Squalene by inhibiting the enzyme Squalene synthase. This has no effect on Mevalonate, or any of the substances listed in the above paragraph. Perfect!
A Squalene synthase inhibitor called Lapaquistat (a.k.a. TAK-475) was developed and tested by Takeda Pharmaceutical Company Limited in 2008. So, why is this wonder drug not on the market today? According to Limited press release - Discontinuation of Development of TAK-475, A Compound for Treatment of Hypercholesterolemia:- " the profile of the compound is not superior to existing marketed drugs from both efficacy and safety viewpoints".
So, just reducing serum cholesterol without changing anything else is not superior to reducing serum cholesterol and changing loads of other things. Maybe statins reduce CHD mortality a bit because they change loads of other things, not because they reduce serum cholesterol. See Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein.
Statins are anti-inflammatory. So is Vitamin D3. I'd take Vitamin D3 instead of statins any day.
Tuesday, 23 March 2010
Saturday, 20 March 2010
Determinants of the Variability in Human Body-fat Percentage.
There are extremely skinny people, very skinny people, skinny people, average people, fat people, very fat people and extremely fat people. However, all healthy newborns have roughly the same body-fat percentage.
As we grow, we gain weight. That's normal. However, the percentage of our bodies that's body-fat can and does change. I'm not going to start another pointless "is a calorie a calorie?" debate as whether it is (as I believe) or it isn't (as others believe), isn't particularly relevant.
What makes some people gain more body-fat mass & less muscle mass than others?
Where nutrients end up depends on the relative insulin sensitivity of the target tissues.
Fat cells are usually always sensitive to insulin unless they are so full of fat that they cannot accommodate any more, in which case either pre-fat cells get turned into new empty fat cells, or if there are no pre-fat cells left, the result is type 2 diabetes.
Muscle cells vary in their sensitivity to insulin. Inactivity lowers insulin sensitivity and intense exercise increases it. Body-builders do a lot of intense exercise so as to maximise muscle cell insulin sensitivity in order to get the maximum amount of nutrients into muscle cells rather than fat cells.
Liver cells vary in their sensitivity to insulin depending on how full of glycogen they are and how much visceral fat (fat around the internal organs) there is.
What makes our weight go up?
1) Eating
2) Drinking
3) Putting on clothes
4) Oxygen breathed in
What makes our weight go down?
1) Defaecating
2) Urinating
3) Taking off clothes
4) Carbon dioxide & water vapour breathed out
5) Energy losses due to movement & heat losses due to conduction, convection, radiation & evaporation
6) Miscellaneous (loss of various bodily fluids, loss of skin cells/hairs/nails, ketones in urine/sweat/breath)
Some factors are controllable/reversible and some aren't. Over a period of 24 hours, our weight goes up and down by a few pounds due to the above factors. Whether our average weight over a 24 hour period changes over the course of days, weeks, months & years depends on the balance between the things that make it go up and the things that make it go down.
Why do we eat & drink what (and as much as) we do?
1) Parents
When we are young, what & how much we eat is determined by our parents (also schools). They dictate the foods and the portion sizes. Poor parents (also schools) often buy the cheapest possible foods. Poor parents encourage "plate-clearing" as they cannot afford waste.
2) Genetics
Some of our ancestors lived in hot countries and some lived in cold countries. Some habitually ate meats and some habitually ate shoots or roots or fruits or grains. This has an effect on our bodies. My ancestors came mostly from Northern Europe which may explain why I achieve better appetite control on a meat-based diet rather than a grain-based diet. The ability to digest lactose (milk sugar) is determined by the habitual milk-drinking in adulthood of our ancestors. Only 4.7% of white English people are lactose-intolerant compared to ~98% of Africans, who would have drunk warm raw milk that had lactase in it.
3) Peer pressure from parents, siblings, friends, business partners & significant others
"Go on! One (more) *insert name of junk food/drink here* won't hurt!"
4) Religion/tradition
It's become commonplace for English people to stuff themselves silly at Christmas, eat lots of chocolate eggs at Easter, pancakes etc.
5) Culture
Certain foods that are very nutritious are either culturally-unacceptable or have fallen out of favour e.g. rabbit/horse/cat/dog-meats & offal (brains, stomachs, lungs, pancreases, hearts, kidneys, bladders, necks, feet).
6) Time
Increasingly busy lives make some people buy pre-prepared meals/snacks which are usually refined carbohydrate-based e.g sandwiches, Subway/Maccy D/BK/KFC. Some workers only have access to vending machine foods & drinks or canteen food which may be of dubious quality. Others blow-out on business lunches.
7) Habit
How many people eat by the clock rather than when they are hungry? School children & many workers have no choice and have to eat at set meal times.
8) Media
There are lots of cookery programmes with celebrity chefs endorsing some diet or other and TV adverts for all sorts of manufactured foods but not many adverts for meat, poultry, fish, eggs, cheese etc (whatever happened to "Beefy & Lamby" & "Go to work on an egg"?). There's always some "expert" telling us what to eat & what not to eat. A lot of mindless eating occurs while watching TV.
9) Physiological & psychological reasons
When we're feeling ill, sad or depressed or have unstable blood glucose levels, we may fancy foods which are high in sugar and fat (mmm, chocolate!). People who are very sedentary and/or lacking sufficient Vitamin D may have unstable blood glucose & insulin levels resulting in extreme lethargy after meals followed by ravenous hunger. People with Anorexia Nervosa often starve themselves or purge after meals.
10) Allergies & intolerances
People avoid foods that make them feel ill.
11) Geography
If we live in a country that grows a lot of a certain foodstuff e.g. rice, wheat, beetroot etc, we are encouraged to eat a lot of that particular foodstuff. When we feel hot, our appetites decrease and when we feel cold, our appetites increase. This is why we don't get fat when we put more clothes on to make ourselves feel warmer.
12) Season
This isn't so relevant, now that most foods are transported around the world and sold in supermarkets, but locally-grown seasonal foods bought from farmers' markets are tasty & nutritious.
13) Boredom
The saying "the Devil makes work for idle hands" applies to our brains & stomachs as well.
14) Exercise
Some people's appetites decrease when they exercise and some increase. I used to fall into the latter category. Over-training at high-intensity on insufficient carbohydrate intake can drain muscle glycogen to the point where muscles rapidly suck glucose from the blood causing low blood glucose. Apart from faints, shakes & sweats, this hugely increases appetite as the brain is crying out for something to raise blood glucose a.s.a.p.
15) Beliefs
Lacto-ovo-vegetarians, pescatarians, vegetarians, vegans etc will not eat certain foods for ethical/moral reasons.
16) Senses
The sight & smell of food & the sound of food cooking can increase our appetites. TV adverts and supermarkets use this to increase sales.
17) Hunger
The emptier the stomach is, the more ghrelin it secretes, which increases our appetites.
18) Comfort
If clothing becomes uncomfortably tight around the waist, that can suppress our appetites. Keep your belt on the same hole, to discourage over-eating.
19) Self Shaming
If we catch sight of our bodies in a mirror and don't like what we see, that can suppress our appetites. People who have Anorexia Nervosa see their bodies as fat/obese when they are actually skinny/emaciated.
20) Societal Shaming
In Japan, it's frowned upon to be too fat. Ditto in "Rich" areas of some countries. Fat-shaming can suppress appetite.
21) Current fatness
As we get fatter, fat cells secrete more leptin, which suppresses our appetites. Very fat people's fat cells secrete so much leptin that the brain can become insensitive to it, resulting in poor appetite suppression.
22) Willpower
Some people find it harder than others to resist the enticements listed above to eat/drink more calorie-dense, nutrient-poor junk.
If I've left anything off this list, feel free to comment. Our bodies are pretty complicated and contain many regulatory Negative Feed-Back (NFB) loops, so we humans have managed to survive famines & disasters over the aeons by our ability to store an excess of proteins, carbohydrates & fats as muscle & body-fat (also food in food-stores) and are now at the top of the food chain (except in lion, tiger, wolf, hyena, bear & shark territory!). Our biggest threat today is excessively-cheap & over-promoted manufactured foods which are calorie-dense & moreish and lifestyles that encourage us to over-eat, under-move and under-sun our skins. When people get too fat, their blood glucose control becomes impaired, which encourages even more over-eating and under-moving, thus creating a vicious circle.
I think that manufactured foods should be taxed and the revenue used to subsidise natural foods. One problem with such a plan is that the Government doesn't always use revenue for the purpose intended e.g. Road Tax. Another problem is in defining manufactured foods e.g. does churning milk to make butter count as manufacturing? Ditto pressing olives to make EVOO? I personally think not, but it's a grey area.
I also think that there should be a ban on the advertising of manufactured foods, as adverts encourage us to buy & consume foods we don't need. Marketing is more persuasive than you think.
See also Eat Less, Move More: Solutions to problems.
As we grow, we gain weight. That's normal. However, the percentage of our bodies that's body-fat can and does change. I'm not going to start another pointless "is a calorie a calorie?" debate as whether it is (as I believe) or it isn't (as others believe), isn't particularly relevant.
What makes some people gain more body-fat mass & less muscle mass than others?
Where nutrients end up depends on the relative insulin sensitivity of the target tissues.
Fat cells are usually always sensitive to insulin unless they are so full of fat that they cannot accommodate any more, in which case either pre-fat cells get turned into new empty fat cells, or if there are no pre-fat cells left, the result is type 2 diabetes.
Muscle cells vary in their sensitivity to insulin. Inactivity lowers insulin sensitivity and intense exercise increases it. Body-builders do a lot of intense exercise so as to maximise muscle cell insulin sensitivity in order to get the maximum amount of nutrients into muscle cells rather than fat cells.
Liver cells vary in their sensitivity to insulin depending on how full of glycogen they are and how much visceral fat (fat around the internal organs) there is.
What makes our weight go up?
1) Eating
2) Drinking
3) Putting on clothes
4) Oxygen breathed in
What makes our weight go down?
1) Defaecating
2) Urinating
3) Taking off clothes
4) Carbon dioxide & water vapour breathed out
5) Energy losses due to movement & heat losses due to conduction, convection, radiation & evaporation
6) Miscellaneous (loss of various bodily fluids, loss of skin cells/hairs/nails, ketones in urine/sweat/breath)
Some factors are controllable/reversible and some aren't. Over a period of 24 hours, our weight goes up and down by a few pounds due to the above factors. Whether our average weight over a 24 hour period changes over the course of days, weeks, months & years depends on the balance between the things that make it go up and the things that make it go down.
Why do we eat & drink what (and as much as) we do?
1) Parents
When we are young, what & how much we eat is determined by our parents (also schools). They dictate the foods and the portion sizes. Poor parents (also schools) often buy the cheapest possible foods. Poor parents encourage "plate-clearing" as they cannot afford waste.
2) Genetics
Some of our ancestors lived in hot countries and some lived in cold countries. Some habitually ate meats and some habitually ate shoots or roots or fruits or grains. This has an effect on our bodies. My ancestors came mostly from Northern Europe which may explain why I achieve better appetite control on a meat-based diet rather than a grain-based diet. The ability to digest lactose (milk sugar) is determined by the habitual milk-drinking in adulthood of our ancestors. Only 4.7% of white English people are lactose-intolerant compared to ~98% of Africans, who would have drunk warm raw milk that had lactase in it.
3) Peer pressure from parents, siblings, friends, business partners & significant others
"Go on! One (more) *insert name of junk food/drink here* won't hurt!"
4) Religion/tradition
It's become commonplace for English people to stuff themselves silly at Christmas, eat lots of chocolate eggs at Easter, pancakes etc.
5) Culture
Certain foods that are very nutritious are either culturally-unacceptable or have fallen out of favour e.g. rabbit/horse/cat/dog-meats & offal (brains, stomachs, lungs, pancreases, hearts, kidneys, bladders, necks, feet).
6) Time
Increasingly busy lives make some people buy pre-prepared meals/snacks which are usually refined carbohydrate-based e.g sandwiches, Subway/Maccy D/BK/KFC. Some workers only have access to vending machine foods & drinks or canteen food which may be of dubious quality. Others blow-out on business lunches.
7) Habit
How many people eat by the clock rather than when they are hungry? School children & many workers have no choice and have to eat at set meal times.
8) Media
There are lots of cookery programmes with celebrity chefs endorsing some diet or other and TV adverts for all sorts of manufactured foods but not many adverts for meat, poultry, fish, eggs, cheese etc (whatever happened to "Beefy & Lamby" & "Go to work on an egg"?). There's always some "expert" telling us what to eat & what not to eat. A lot of mindless eating occurs while watching TV.
9) Physiological & psychological reasons
When we're feeling ill, sad or depressed or have unstable blood glucose levels, we may fancy foods which are high in sugar and fat (mmm, chocolate!). People who are very sedentary and/or lacking sufficient Vitamin D may have unstable blood glucose & insulin levels resulting in extreme lethargy after meals followed by ravenous hunger. People with Anorexia Nervosa often starve themselves or purge after meals.
10) Allergies & intolerances
People avoid foods that make them feel ill.
11) Geography
If we live in a country that grows a lot of a certain foodstuff e.g. rice, wheat, beetroot etc, we are encouraged to eat a lot of that particular foodstuff. When we feel hot, our appetites decrease and when we feel cold, our appetites increase. This is why we don't get fat when we put more clothes on to make ourselves feel warmer.
12) Season
This isn't so relevant, now that most foods are transported around the world and sold in supermarkets, but locally-grown seasonal foods bought from farmers' markets are tasty & nutritious.
13) Boredom
The saying "the Devil makes work for idle hands" applies to our brains & stomachs as well.
14) Exercise
Some people's appetites decrease when they exercise and some increase. I used to fall into the latter category. Over-training at high-intensity on insufficient carbohydrate intake can drain muscle glycogen to the point where muscles rapidly suck glucose from the blood causing low blood glucose. Apart from faints, shakes & sweats, this hugely increases appetite as the brain is crying out for something to raise blood glucose a.s.a.p.
15) Beliefs
Lacto-ovo-vegetarians, pescatarians, vegetarians, vegans etc will not eat certain foods for ethical/moral reasons.
16) Senses
The sight & smell of food & the sound of food cooking can increase our appetites. TV adverts and supermarkets use this to increase sales.
17) Hunger
The emptier the stomach is, the more ghrelin it secretes, which increases our appetites.
18) Comfort
If clothing becomes uncomfortably tight around the waist, that can suppress our appetites. Keep your belt on the same hole, to discourage over-eating.
19) Self Shaming
If we catch sight of our bodies in a mirror and don't like what we see, that can suppress our appetites. People who have Anorexia Nervosa see their bodies as fat/obese when they are actually skinny/emaciated.
20) Societal Shaming
In Japan, it's frowned upon to be too fat. Ditto in "Rich" areas of some countries. Fat-shaming can suppress appetite.
21) Current fatness
As we get fatter, fat cells secrete more leptin, which suppresses our appetites. Very fat people's fat cells secrete so much leptin that the brain can become insensitive to it, resulting in poor appetite suppression.
22) Willpower
Some people find it harder than others to resist the enticements listed above to eat/drink more calorie-dense, nutrient-poor junk.
If I've left anything off this list, feel free to comment. Our bodies are pretty complicated and contain many regulatory Negative Feed-Back (NFB) loops, so we humans have managed to survive famines & disasters over the aeons by our ability to store an excess of proteins, carbohydrates & fats as muscle & body-fat (also food in food-stores) and are now at the top of the food chain (except in lion, tiger, wolf, hyena, bear & shark territory!). Our biggest threat today is excessively-cheap & over-promoted manufactured foods which are calorie-dense & moreish and lifestyles that encourage us to over-eat, under-move and under-sun our skins. When people get too fat, their blood glucose control becomes impaired, which encourages even more over-eating and under-moving, thus creating a vicious circle.
I think that manufactured foods should be taxed and the revenue used to subsidise natural foods. One problem with such a plan is that the Government doesn't always use revenue for the purpose intended e.g. Road Tax. Another problem is in defining manufactured foods e.g. does churning milk to make butter count as manufacturing? Ditto pressing olives to make EVOO? I personally think not, but it's a grey area.
I also think that there should be a ban on the advertising of manufactured foods, as adverts encourage us to buy & consume foods we don't need. Marketing is more persuasive than you think.
See also Eat Less, Move More: Solutions to problems.
Tuesday, 16 March 2010
How many working brain cells do researchers have? Part 2.
Having discovered The Cochrane Library, I thought I'd see what was in it regarding Vitamin D & Cancer. I found the following Protocol Vitamin D supplementation for prevention of cancer in adults.
"Why it is important to do this review
The available evidence on vitamin D and cancer incidence is intriguing but inconclusive. Results of recently completed randomised clinical trials testing the influence of vitamin D supplementation for cancer prevention are inconsistent. Lappe et al found that vitamin D supplementation is associated with significantly decreased cancer incidence (Lappe 2007). On the contrary, another large randomised clinical trial found no effect of vitamin D and calcium supplementation on cancer incidence (Wactawski-Wende 2006). A recent meta-analysis by Autier and Gandini of 18 randomised clinical trials found significantly lower mortality in vitamin D supplemented participants (Autier 2007). We have been unable to identify any systematic reviews of randomised trials on vitamin D supplementation for cancer prevention."
I took a closer look at the Wactawski-Wende trial. In this trial, a daily Vitamin D dose of 400IU was used. That's less than one tenth of an effective dose (5,000IU/day). What happens when you take less than one tenth of an effective dose of a medication? Nothing. Which is exactly what they found. Like, Duh!
The randomised trials in the Autier meta-analysis used daily Vitamin D doses of 300 to 2000IU. The trial size–adjusted mean daily vitamin D dose was 528IU. Once again, mostly pathetically inadequate doses were used.
The Lappe trial used a daily Vitamin D dose of 1,100IU (+ Calcium). It's a bit low, but there was a beneficial effect. When analysis was confined to cancers diagnosed after the first 12 months (to allow time for serum 25(OH)D levels to stabilise and ignore results from subjects who started the trial with undiagnosed cancers), there was a 77% reduction in cancer diagnoses (RR for the Ca + D group fell to 0.232 (CI: 0.09, 0.60; P < 0.005)).
No cancer trials have yet been done using 5,000IU/day of Vitamin D3.
So, thanks to eejit researchers testing ineffective doses, there is no conclusive evidence supporting Vitamin D3. People continue to die from cancer unnecessarily. What is Cancer Research doing with all of the money that they get?
"Why it is important to do this review
The available evidence on vitamin D and cancer incidence is intriguing but inconclusive. Results of recently completed randomised clinical trials testing the influence of vitamin D supplementation for cancer prevention are inconsistent. Lappe et al found that vitamin D supplementation is associated with significantly decreased cancer incidence (Lappe 2007). On the contrary, another large randomised clinical trial found no effect of vitamin D and calcium supplementation on cancer incidence (Wactawski-Wende 2006). A recent meta-analysis by Autier and Gandini of 18 randomised clinical trials found significantly lower mortality in vitamin D supplemented participants (Autier 2007). We have been unable to identify any systematic reviews of randomised trials on vitamin D supplementation for cancer prevention."
I took a closer look at the Wactawski-Wende trial. In this trial, a daily Vitamin D dose of 400IU was used. That's less than one tenth of an effective dose (5,000IU/day). What happens when you take less than one tenth of an effective dose of a medication? Nothing. Which is exactly what they found. Like, Duh!
The randomised trials in the Autier meta-analysis used daily Vitamin D doses of 300 to 2000IU. The trial size–adjusted mean daily vitamin D dose was 528IU. Once again, mostly pathetically inadequate doses were used.
The Lappe trial used a daily Vitamin D dose of 1,100IU (+ Calcium). It's a bit low, but there was a beneficial effect. When analysis was confined to cancers diagnosed after the first 12 months (to allow time for serum 25(OH)D levels to stabilise and ignore results from subjects who started the trial with undiagnosed cancers), there was a 77% reduction in cancer diagnoses (RR for the Ca + D group fell to 0.232 (CI: 0.09, 0.60; P < 0.005)).
No cancer trials have yet been done using 5,000IU/day of Vitamin D3.
So, thanks to eejit researchers testing ineffective doses, there is no conclusive evidence supporting Vitamin D3. People continue to die from cancer unnecessarily. What is Cancer Research doing with all of the money that they get?
Sunday, 14 March 2010
Dementia: A review of the evidence.
To make my discussions with Health Professionals a.k.a. "experts" more effective, I need to know what they know. To help me with this task, I have been rummaging through The Cochrane Library. The results for Dementia NOT "Down Syndrome" NOT Vascular NOT Aids NOT carer and Reviews only produced 44 results. Some weren't relevant. The following are relevant and I have added the plain language summary:-
Acetyl-l-carnitine for dementia. No evidence of benefit of Acetyl-l-carnitine for dementia.
Alpha lipoic acid for dementia. No evidence of efficacy of alpha lipoic acid for dementia.
Antidepressants for treating depression in dementia. Insufficient evidence for the efficacy and safety of antidepressants for depression in dementia.
Aroma therapy for dementia. The one small trial published is insufficient evidence for the efficacy of aroma therapy for dementia.
Cannabinoids for the treatment of dementia. No evidence that cannabinoids are effective in the improvement of disturbed behaviour in dementia or in the treatment of other symptoms of dementia.
Cholinesterase inhibitors for dementia with Lewy bodies. No convincing evidence from one trial of the efficacy of cholinesterase inhibitors for dementia with Lewy bodies.
Cholinesterase inhibitors for Parkinson's disease dementia. Rivastigmine appears to moderately improve cognition and to a lesser extent activities of daily living in patients with PDD.
Donepezil for dementia due to Alzheimer's disease. Donepezil is beneficial for people with mild, moderate and severe dementia due to Alzheimer's disease.
Ginkgo biloba for cognitive impairment and dementia. There is no convincing evidence that Ginkgo biloba is efficacious for dementia and cognitive impairment.
Haloperidol for agitation in dementia. No evidence has been found of any significant general improvement in manifestations of agitation, other than aggression, among demented patients treated with haloperidol, compared with controls.
Homeopathy for dementia. No evidence that homeopathy is effective in treating dementia.
Hormone replacement therapy to maintain cognitive function in women with dementia. There is no evidence of a positive effect that oestrogen replacement therapy can maintain cognitive function for a longer period of time (> five months) in women with Alzheimer's disease.
Hydergine for dementia. Uncertainty about the efficacy of hydergine in dementia.
Lecithin for dementia and cognitive impairment. Doubtful effect of lecithin as a treatment for dementia.
Light therapy for managing cognitive, sleep, functional, behavioural, or psychiatric disturbances in dementia. There is insufficient evidence to determine whether light therapy is effective in the management of cognitive, sleep, functional, behavioural or psychiatric disturbances in dementia.
Massage and touch for dementia. Insufficient evidence to draw conclusions about the possibility that massage and touch interventions are effective for dementia or associated problems.
Memantine for dementia. Some evidence of efficacy of memantine for dementia.
Music therapy for people with dementia. There is no substantial evidence to support nor discourage the use of music therapy in the care of older people with dementia.
Nicergoline for dementia and other age associated forms of cognitive impairment. Nicergoline may improve cognition and behavioural function of people with mild to moderate dementia.
Omega 3 fatty acid for the prevention of dementia. There is no evidence that dietary or supplemental omega 3 polyunsaturated fatty acid (PUFA) reduces the risk of cognitive impairment or dementia in healthy elderly persons without pre-existing dementia. This review yielded no clinical trials that could confirm or refute the utility of omega 3 PUFA in preventing cognitive impairment or dementia. This is an important area that is in pressing need of further research.
Physical activity programs for persons with dementia. There is insufficient evidence to determine the effectiveness of physical activity programs in managing or improving cognition, function, behaviour, depression, and mortality in people with dementia.
Physostigmine for dementia due to Alzheimer's disease. Limited evidence of effectiveness of physostigmine for the symptomatic treatment of Alzheimer's disease.
Piracetam for dementia or cognitive impairment. Evidence for the efficacy of piracetam for dementia or cognitive impairment is inadequate for clinical use but sufficient to justify further research.
Procaine treatments for cognition and dementia. In analysing the effect of procaine and its preparations, there was no evidence for benefit in the prevention or treatment of dementia or cognitive impairment.
Propentofylline for dementia. Limited evidence that propentofylline benefits cognition, global function and activities of daily living in people with Alzheimer's disease and/or vascular dementia.
Reminiscence therapy for dementia. Inconclusive evidence of the efficacy of reminiscence therapy for dementia.
Snoezelen for dementia. No evidence of the efficacy of snoezelen or multi-sensory stimulation programmes for people with dementia.
Statins for the prevention of dementia. There (is) good evidence that statins given in late life to individuals at risk of vascular disease have no effect in preventing dementia.
Thioridazine for dementia. No evidence to support the use of thioridazine for dementia.
Transcutaneous Electrical Nerve Stimulation (TENS) for dementia. Insufficient data to determine the efficacy of transcutaneous electrical nerve stimulation for dementia.
Trazodone for agitation in dementia. Insufficient evidence from randomized, placebo-controlled studies to support a recommendation that trazodone should be prescribed, or not prescribed, for BPSD.
Validation therapy for dementia. No new evidence of the efficacy of validation therapy for people with dementia or cognitive impairment has been identified.
Valproate preparations for agitation in dementia. No evidence of efficacy of valproate preparations for treatment of agitation in people with dementia.
Vinpocetine for cognitive impairment and dementia. Insufficient evidence of benefits of vinpocetine for people with dementia.
So there you have it. Virtually everything that's been thoroughly tested is ineffective for the treatment of dementia.
There are a whole load of things that haven't been properly tested yet e.g. Omega-3, Vitamin D3, Vitamin K2, Curcumin, Berberine, Trans-dermal Progesterone, Sub-lingual B12, S-Adeno-Methionine and The Ketogenic Diet. What is The Alzheimer's Society doing with all of the money that they get?
Finally, I accept that mum is on her last legs and won't be around for much longer, so here's a song. I normally hate raps, but the Pinky & Perky backing vocals are kinda quirky and the lyrics are poignant. So here's Stay with Me by DJ Ironik. Listen to the words!
Acetyl-l-carnitine for dementia. No evidence of benefit of Acetyl-l-carnitine for dementia.
Alpha lipoic acid for dementia. No evidence of efficacy of alpha lipoic acid for dementia.
Antidepressants for treating depression in dementia. Insufficient evidence for the efficacy and safety of antidepressants for depression in dementia.
Aroma therapy for dementia. The one small trial published is insufficient evidence for the efficacy of aroma therapy for dementia.
Cannabinoids for the treatment of dementia. No evidence that cannabinoids are effective in the improvement of disturbed behaviour in dementia or in the treatment of other symptoms of dementia.
Cholinesterase inhibitors for dementia with Lewy bodies. No convincing evidence from one trial of the efficacy of cholinesterase inhibitors for dementia with Lewy bodies.
Cholinesterase inhibitors for Parkinson's disease dementia. Rivastigmine appears to moderately improve cognition and to a lesser extent activities of daily living in patients with PDD.
Donepezil for dementia due to Alzheimer's disease. Donepezil is beneficial for people with mild, moderate and severe dementia due to Alzheimer's disease.
Ginkgo biloba for cognitive impairment and dementia. There is no convincing evidence that Ginkgo biloba is efficacious for dementia and cognitive impairment.
Haloperidol for agitation in dementia. No evidence has been found of any significant general improvement in manifestations of agitation, other than aggression, among demented patients treated with haloperidol, compared with controls.
Homeopathy for dementia. No evidence that homeopathy is effective in treating dementia.
Hormone replacement therapy to maintain cognitive function in women with dementia. There is no evidence of a positive effect that oestrogen replacement therapy can maintain cognitive function for a longer period of time (> five months) in women with Alzheimer's disease.
Hydergine for dementia. Uncertainty about the efficacy of hydergine in dementia.
Lecithin for dementia and cognitive impairment. Doubtful effect of lecithin as a treatment for dementia.
Light therapy for managing cognitive, sleep, functional, behavioural, or psychiatric disturbances in dementia. There is insufficient evidence to determine whether light therapy is effective in the management of cognitive, sleep, functional, behavioural or psychiatric disturbances in dementia.
Massage and touch for dementia. Insufficient evidence to draw conclusions about the possibility that massage and touch interventions are effective for dementia or associated problems.
Memantine for dementia. Some evidence of efficacy of memantine for dementia.
Music therapy for people with dementia. There is no substantial evidence to support nor discourage the use of music therapy in the care of older people with dementia.
Nicergoline for dementia and other age associated forms of cognitive impairment. Nicergoline may improve cognition and behavioural function of people with mild to moderate dementia.
Omega 3 fatty acid for the prevention of dementia. There is no evidence that dietary or supplemental omega 3 polyunsaturated fatty acid (PUFA) reduces the risk of cognitive impairment or dementia in healthy elderly persons without pre-existing dementia. This review yielded no clinical trials that could confirm or refute the utility of omega 3 PUFA in preventing cognitive impairment or dementia. This is an important area that is in pressing need of further research.
Physical activity programs for persons with dementia. There is insufficient evidence to determine the effectiveness of physical activity programs in managing or improving cognition, function, behaviour, depression, and mortality in people with dementia.
Physostigmine for dementia due to Alzheimer's disease. Limited evidence of effectiveness of physostigmine for the symptomatic treatment of Alzheimer's disease.
Piracetam for dementia or cognitive impairment. Evidence for the efficacy of piracetam for dementia or cognitive impairment is inadequate for clinical use but sufficient to justify further research.
Procaine treatments for cognition and dementia. In analysing the effect of procaine and its preparations, there was no evidence for benefit in the prevention or treatment of dementia or cognitive impairment.
Propentofylline for dementia. Limited evidence that propentofylline benefits cognition, global function and activities of daily living in people with Alzheimer's disease and/or vascular dementia.
Reminiscence therapy for dementia. Inconclusive evidence of the efficacy of reminiscence therapy for dementia.
Snoezelen for dementia. No evidence of the efficacy of snoezelen or multi-sensory stimulation programmes for people with dementia.
Statins for the prevention of dementia. There (is) good evidence that statins given in late life to individuals at risk of vascular disease have no effect in preventing dementia.
Thioridazine for dementia. No evidence to support the use of thioridazine for dementia.
Transcutaneous Electrical Nerve Stimulation (TENS) for dementia. Insufficient data to determine the efficacy of transcutaneous electrical nerve stimulation for dementia.
Trazodone for agitation in dementia. Insufficient evidence from randomized, placebo-controlled studies to support a recommendation that trazodone should be prescribed, or not prescribed, for BPSD.
Validation therapy for dementia. No new evidence of the efficacy of validation therapy for people with dementia or cognitive impairment has been identified.
Valproate preparations for agitation in dementia. No evidence of efficacy of valproate preparations for treatment of agitation in people with dementia.
Vinpocetine for cognitive impairment and dementia. Insufficient evidence of benefits of vinpocetine for people with dementia.
So there you have it. Virtually everything that's been thoroughly tested is ineffective for the treatment of dementia.
There are a whole load of things that haven't been properly tested yet e.g. Omega-3, Vitamin D3, Vitamin K2, Curcumin, Berberine, Trans-dermal Progesterone, Sub-lingual B12, S-Adeno-Methionine and The Ketogenic Diet. What is The Alzheimer's Society doing with all of the money that they get?
Finally, I accept that mum is on her last legs and won't be around for much longer, so here's a song. I normally hate raps, but the Pinky & Perky backing vocals are kinda quirky and the lyrics are poignant. So here's Stay with Me by DJ Ironik. Listen to the words!
Friday, 12 March 2010
"Experts"...again!
As mentioned in A slight hitch, Part 2., I attended a "robust" meeting with social services, representatives of the nursing home, mum's Community Psychiatric Nurse and mum's Memory Clinic consultant. Although the meeting didn't go quite as I'd hoped, the outcome was good as the standard of care at the nursing home has improved. She's moving to a better nursing home on Monday 15th March anyway as I'd had enough of the shenanigans with the management that runs the current nursing home.
After the meeting, I had a long chat with mum's Memory Clinic consultant. He explained that I couldn't give mum supplements based on weak evidence e.g. in-vitro studies, animal studies or epidemiological/observational human studies showing associations between "A" & "B". There had to be a sufficient number of large Randomised Controlled Trials (RCTs). Fair enough.
I recently e-mailed the consultant including a couple of links to RCTs showing the positive effect of Vitamin D3 on mood. He e-mailed back saying that the evidence was still weak and he linked me to The Cochrane Collaboration web-site and also to the book Evidence Based Medicine - How to Practice and Teach EBM. I bought the book and took a look at the web-site.
Due to a bug on Amazon, looking inside the above book showed me a completely different book which contained a very interesting piece of information.
The Flecainide Story
Pre-Ventricular Contractions (PVCs) are a fancy name for cardiac arrhythmias. PVCs often result in Ventricular Fibrillation (VF) & death during heart attacks. A crossover study done in the US in the 1980s showed that Flecainide drastically reduced PVCs compared to placebo. Flecainide was approved by the US Food & Drugs Administration (FDA) and prescribed to hundreds of thousands of American heart attack patients (though it never caught on in Europe or Australia).
Unfortunately a later study, the Cardiac Arrhythmia Suppression Trial (CAST) showed that, over an 18 month period, about 12% of patients taking Flecainide died compared to about 5% of patients taking placebo. Oh, whoops! It took quite a while for the bad news to be accepted (as nobody likes bad news especially when it adversely affects drug sales & profits) and for Flecainide to be taken off the market. In the meantime, tens of thousands of Americans died unnecessarily. This is what happens when "experts" focus on one outcome only and ignore the rather more important outcome of all-cause mortality.
Statins reduce cardiac deaths in men under 50 who have had one or more heart attacks. There's a statistically-insignificant reduction in all-cause mortality though as deaths from other causes increase. There's also no statistically-significant all-cause mortality benefit to men over 50 or all women who have had one or more heart attacks, or people who haven't had a heart attack. However, that hasn't stopped statins being prescribed to all and sundry, whether young or old, whether male or female and whether having had a heart attack or not.
The Cochrane Collaboration web-site was most interesting. During my long chat with mum's Memory Clinic consultant, he explained that mum was prescribed a cholinesterase inhibitor (Donepezil a.k.a. Aricept) as there was strong evidence for its benefit. I found Donepezil for dementia due to Alzheimer's disease which indeed confirmed the benefit to patients with Alzheimer's Disease (AD). The thing is, mum doesn't have AD. She has Dementia with Lewy Bodies (DLB). I then found Cholinesterase inhibitors for dementia with Lewy bodies, which concluded:-
"Patients with dementia with Lewy bodies who suffer from behavioural disturbance or psychiatric problems may benefit from rivastigmine if they tolerate it, but the evidence is weak." (emphasis added by me).
There is a condition called Parkinson's Disease Dementia (PDD) which is similar (but not identical) to DLB and I found Cholinesterase inhibitors for Parkinson's disease dementia which concluded:-
"Rivastigmine appears to improve cognition and activities of daily living in patients with PDD."
Rivastigmine is similar (but not identical) to Donepezil. There were no reviews showing the effect of Donepezil on DLB.
So "experts" can prescribe medications based on weak/no evidence but I can't give mum supplements based on weak evidence. I'm not going to e-mail the consultant pointing this out as he may withdraw Donepezil and it does actually have a slight benefit. I'm going to print the above studies and use them to try to persuade mum's new GP (when mum's moved to the new nursing home) to permit me to supply mum with supplements based on my evidence.
I also found Omega 3 fatty acid for the prevention of dementia which stated:-
"Background
Accruing evidence from observational and epidemiological studies suggests an inverse relationship between dietary intake of omega 3 polyunsaturated fatty acid (PUFA) and risk of dementia. Postulated mechanisms that might qualify omega 3 PUFA as an interventional target for the primary prevention of dementia include its anti-atherogenic, anti-inflammatory, anti-oxidant, anti-amyloid and neuroprotective properties.
Main results
There were no randomized trials found in the search that met the selection criteria. Results of two clinical trials are expected in 2008.
Authors' conclusions
There is a growing body of evidence from biological, observational and epidemiological studies that suggests a protective effect of omega 3 PUFA against dementia. However, until data from randomized trials become available for analysis, there is no good evidence to support the use of dietary or supplemental omega 3 PUFA for the prevention of cognitive impairment or dementia."
It's now 2010 and there are still no results from RCTs showing. So, omega-3 PUFAs will not be prescribed despite the evidence from biological, observational and epidemiological studies. Luckily, I keep mum's mini-fridge stocked with smoked salmon and I will request that the new nursing home gives mum a salmon meal twice a week.
After the meeting, I had a long chat with mum's Memory Clinic consultant. He explained that I couldn't give mum supplements based on weak evidence e.g. in-vitro studies, animal studies or epidemiological/observational human studies showing associations between "A" & "B". There had to be a sufficient number of large Randomised Controlled Trials (RCTs). Fair enough.
I recently e-mailed the consultant including a couple of links to RCTs showing the positive effect of Vitamin D3 on mood. He e-mailed back saying that the evidence was still weak and he linked me to The Cochrane Collaboration web-site and also to the book Evidence Based Medicine - How to Practice and Teach EBM. I bought the book and took a look at the web-site.
Due to a bug on Amazon, looking inside the above book showed me a completely different book which contained a very interesting piece of information.
The Flecainide Story
Pre-Ventricular Contractions (PVCs) are a fancy name for cardiac arrhythmias. PVCs often result in Ventricular Fibrillation (VF) & death during heart attacks. A crossover study done in the US in the 1980s showed that Flecainide drastically reduced PVCs compared to placebo. Flecainide was approved by the US Food & Drugs Administration (FDA) and prescribed to hundreds of thousands of American heart attack patients (though it never caught on in Europe or Australia).
Unfortunately a later study, the Cardiac Arrhythmia Suppression Trial (CAST) showed that, over an 18 month period, about 12% of patients taking Flecainide died compared to about 5% of patients taking placebo. Oh, whoops! It took quite a while for the bad news to be accepted (as nobody likes bad news especially when it adversely affects drug sales & profits) and for Flecainide to be taken off the market. In the meantime, tens of thousands of Americans died unnecessarily. This is what happens when "experts" focus on one outcome only and ignore the rather more important outcome of all-cause mortality.
Statins reduce cardiac deaths in men under 50 who have had one or more heart attacks. There's a statistically-insignificant reduction in all-cause mortality though as deaths from other causes increase. There's also no statistically-significant all-cause mortality benefit to men over 50 or all women who have had one or more heart attacks, or people who haven't had a heart attack. However, that hasn't stopped statins being prescribed to all and sundry, whether young or old, whether male or female and whether having had a heart attack or not.
The Cochrane Collaboration web-site was most interesting. During my long chat with mum's Memory Clinic consultant, he explained that mum was prescribed a cholinesterase inhibitor (Donepezil a.k.a. Aricept) as there was strong evidence for its benefit. I found Donepezil for dementia due to Alzheimer's disease which indeed confirmed the benefit to patients with Alzheimer's Disease (AD). The thing is, mum doesn't have AD. She has Dementia with Lewy Bodies (DLB). I then found Cholinesterase inhibitors for dementia with Lewy bodies, which concluded:-
"Patients with dementia with Lewy bodies who suffer from behavioural disturbance or psychiatric problems may benefit from rivastigmine if they tolerate it, but the evidence is weak." (emphasis added by me).
There is a condition called Parkinson's Disease Dementia (PDD) which is similar (but not identical) to DLB and I found Cholinesterase inhibitors for Parkinson's disease dementia which concluded:-
"Rivastigmine appears to improve cognition and activities of daily living in patients with PDD."
Rivastigmine is similar (but not identical) to Donepezil. There were no reviews showing the effect of Donepezil on DLB.
So "experts" can prescribe medications based on weak/no evidence but I can't give mum supplements based on weak evidence. I'm not going to e-mail the consultant pointing this out as he may withdraw Donepezil and it does actually have a slight benefit. I'm going to print the above studies and use them to try to persuade mum's new GP (when mum's moved to the new nursing home) to permit me to supply mum with supplements based on my evidence.
I also found Omega 3 fatty acid for the prevention of dementia which stated:-
"Background
Accruing evidence from observational and epidemiological studies suggests an inverse relationship between dietary intake of omega 3 polyunsaturated fatty acid (PUFA) and risk of dementia. Postulated mechanisms that might qualify omega 3 PUFA as an interventional target for the primary prevention of dementia include its anti-atherogenic, anti-inflammatory, anti-oxidant, anti-amyloid and neuroprotective properties.
Main results
There were no randomized trials found in the search that met the selection criteria. Results of two clinical trials are expected in 2008.
Authors' conclusions
There is a growing body of evidence from biological, observational and epidemiological studies that suggests a protective effect of omega 3 PUFA against dementia. However, until data from randomized trials become available for analysis, there is no good evidence to support the use of dietary or supplemental omega 3 PUFA for the prevention of cognitive impairment or dementia."
It's now 2010 and there are still no results from RCTs showing. So, omega-3 PUFAs will not be prescribed despite the evidence from biological, observational and epidemiological studies. Luckily, I keep mum's mini-fridge stocked with smoked salmon and I will request that the new nursing home gives mum a salmon meal twice a week.
Tuesday, 9 March 2010
I am NOT the anti-carb!
On a messageboard far, far away I was told:-
"While cakes and biscuits might be regarded primarily as treats, bread and pasta are staple foods, which form an important part of the diet of growing children, who are recommended by experts to get a fairly high proportion of their calories from carbohydrates, including wheat flour.
It is normal and healthy for children to have sandwiches and pasta as part of their meals, and pizza and pastry in moderation are perfectly appropriate. As are occasional treats.
I don’t suppose that I am the only person who is tired of your ceaseless evangelising on behalf of your own diet. But it is one thing to feed yourself as you please, and to talk about it if you wish, it is quite another to suggest that there is good reason for people to adopt your personal principles and ignore the advice of paediatricians, dieticians, and properly constituted advisory bodies when feeding children."
Also
"I'm sorry Nigel, but you do give the impression of being on a one man crusade against wheat in our diets. You are also making the assumption that we all eat refined wheat. What about wholemeal bread, wholegrain cereals, wholemeal pasta? You are also assuming that we all buy sliced white bread. I make most of my bread in my bread machine, using organic flour. I know what goes into my bread, and it tastes so much better than supermarket bread.
Pasta need not be made from wheat, for example rice noodles and rice and corn pasta for coeliacs.
So many cuisines have wheat products in their diets. Obviously there are the different breads - nan, pitta, flatbread, tortilla wraps etc; a huge array of pastas, cous-cous; bulgar wheat. Wheat is also used in so many religious/celebratory foods - the bread at holy communion, Christmas/simnel/birthday cakes etc. I could go on."
Plus
"Most widespread cultures have one or two staple carbohydrates, predominantly grains, that are the basis of the normal healthy diet.
In Europe and Northern American those staples are wheat and potatoes. It is hence making a rod for your own back, and entirely unnecessary, to try to feed a child without both of these unless they have specific issues such as Coeliac disease - ask the parent of such a child just how difficult it is. Your argument that the eating of wheat is what makes westerners fat is entirely specious, as few of the more lean members of the culture have eschewed wheat, and your suggestion that the recommendations based on the food pyramid have failed at the population has got more obese since the pyramid was devised is a twisting of the facts – all the relaible evidence shows that the people who stick to the recommendations are just fine, it’s those that don’t follow the guidelines who become obese. The guidance in no way is a cause of the obesity epidemic.
In most of Asia the staple is rice (which, as eaten, is a refined grain incidentally, I don't know why you think it isn't)."
The above raises so many points that it's hard to know where to start. The beginning is probably the best place. WARNING! The following contains some irony.
"Experts" tell us what we should and shouldn't eat. That's worked so well, hasn't it? It's easy to blame people for not following the very guidelines that make them over-eat. It's their own stupid fault! "Experts" scoffed at Dr. Ignaz Semmelweis. He was more right than wrong though and modern medicine now uses sterile practices. "Experts" scoffed at James Lind and it took 42 years before the British navy adopted lemons or limes as standard issue at sea. So we know where "experts" can shove their dietary advice ... somewhere where the sun doesn't synthesise Vitamin D.
I don't try to get everybody on a low-carb diet. Jeez! Firstly, we are not all the same. Everyone has a different requirement for carbohydrate. As I wrote in Carbohydrates: Dogs' Doodads or Spawn of Satan?, "Right carbs, right amounts, right times." People don't do this, though. They eat the wrong carbs (powdered grains, mashed potato & other over-refined carbs like fruit juice) in the wrong amounts (way too much, as per "expert" advice) at the wrong times (virtually every meal, whether active or sedentary). Some random musings...
WHEATFLOUR: I guess it must be the lack of wheatflour that's pushed Orientals to the verge of extinction. Oh, wait...
LONGEVITY: Turn the clock back to a time before modern medicine and we wheatflour eaters had long average lifespans. Oh, wait...
BREAD: The vast majority of bread bought today is muck, mass-produced by the Chorleywood Bread Process. Even home-made bread is made from grain dust. See The problem with "Whole Grain" cereal etc. I don't consider white rice to be a refined grain as it still looks like a grain.
PASTA: When I was a lad, the only pasta we had was Heinz Spaghetti & Ravioli in tomato sauce. Now, pasta is a staple food in the UK? We all know how slim middle-aged Italians are. Oh, wait...
EXERCISE: When I was a lad, I used to run around in the street & playground like other kids. I was still fat. Exercise cannot compensate for poor diet (I ate lots of chocolate, cake & drank sugary Corona lemonade).
Why do we have to eat what farmers grow? Maybe if more people ate less powdered wheat products and more old-fashioned sourdough rye bread, farmers might start growing something else. There are plenty of carbohydrates that don't seriously disturb blood glucose levels, such as rice, rye, barley, quinoa, sorghum, millet, maize, sago, tubers, root veggies, bulbs, legumes & fresh whole fruits.
Nah, it'll never happen! Not while a) crap foods are dirt cheap and b) people keep following the dietary advice of "experts" like sheep ... or should that be lemmings?
See also Anthony Colpo's The Whole Grain Scam.
"While cakes and biscuits might be regarded primarily as treats, bread and pasta are staple foods, which form an important part of the diet of growing children, who are recommended by experts to get a fairly high proportion of their calories from carbohydrates, including wheat flour.
It is normal and healthy for children to have sandwiches and pasta as part of their meals, and pizza and pastry in moderation are perfectly appropriate. As are occasional treats.
I don’t suppose that I am the only person who is tired of your ceaseless evangelising on behalf of your own diet. But it is one thing to feed yourself as you please, and to talk about it if you wish, it is quite another to suggest that there is good reason for people to adopt your personal principles and ignore the advice of paediatricians, dieticians, and properly constituted advisory bodies when feeding children."
Also
"I'm sorry Nigel, but you do give the impression of being on a one man crusade against wheat in our diets. You are also making the assumption that we all eat refined wheat. What about wholemeal bread, wholegrain cereals, wholemeal pasta? You are also assuming that we all buy sliced white bread. I make most of my bread in my bread machine, using organic flour. I know what goes into my bread, and it tastes so much better than supermarket bread.
Pasta need not be made from wheat, for example rice noodles and rice and corn pasta for coeliacs.
So many cuisines have wheat products in their diets. Obviously there are the different breads - nan, pitta, flatbread, tortilla wraps etc; a huge array of pastas, cous-cous; bulgar wheat. Wheat is also used in so many religious/celebratory foods - the bread at holy communion, Christmas/simnel/birthday cakes etc. I could go on."
Plus
"Most widespread cultures have one or two staple carbohydrates, predominantly grains, that are the basis of the normal healthy diet.
In Europe and Northern American those staples are wheat and potatoes. It is hence making a rod for your own back, and entirely unnecessary, to try to feed a child without both of these unless they have specific issues such as Coeliac disease - ask the parent of such a child just how difficult it is. Your argument that the eating of wheat is what makes westerners fat is entirely specious, as few of the more lean members of the culture have eschewed wheat, and your suggestion that the recommendations based on the food pyramid have failed at the population has got more obese since the pyramid was devised is a twisting of the facts – all the relaible evidence shows that the people who stick to the recommendations are just fine, it’s those that don’t follow the guidelines who become obese. The guidance in no way is a cause of the obesity epidemic.
In most of Asia the staple is rice (which, as eaten, is a refined grain incidentally, I don't know why you think it isn't)."
The above raises so many points that it's hard to know where to start. The beginning is probably the best place. WARNING! The following contains some irony.
"Experts" tell us what we should and shouldn't eat. That's worked so well, hasn't it? It's easy to blame people for not following the very guidelines that make them over-eat. It's their own stupid fault! "Experts" scoffed at Dr. Ignaz Semmelweis. He was more right than wrong though and modern medicine now uses sterile practices. "Experts" scoffed at James Lind and it took 42 years before the British navy adopted lemons or limes as standard issue at sea. So we know where "experts" can shove their dietary advice ... somewhere where the sun doesn't synthesise Vitamin D.
I don't try to get everybody on a low-carb diet. Jeez! Firstly, we are not all the same. Everyone has a different requirement for carbohydrate. As I wrote in Carbohydrates: Dogs' Doodads or Spawn of Satan?, "Right carbs, right amounts, right times." People don't do this, though. They eat the wrong carbs (powdered grains, mashed potato & other over-refined carbs like fruit juice) in the wrong amounts (way too much, as per "expert" advice) at the wrong times (virtually every meal, whether active or sedentary). Some random musings...
WHEATFLOUR: I guess it must be the lack of wheatflour that's pushed Orientals to the verge of extinction. Oh, wait...
LONGEVITY: Turn the clock back to a time before modern medicine and we wheatflour eaters had long average lifespans. Oh, wait...
BREAD: The vast majority of bread bought today is muck, mass-produced by the Chorleywood Bread Process. Even home-made bread is made from grain dust. See The problem with "Whole Grain" cereal etc. I don't consider white rice to be a refined grain as it still looks like a grain.
PASTA: When I was a lad, the only pasta we had was Heinz Spaghetti & Ravioli in tomato sauce. Now, pasta is a staple food in the UK? We all know how slim middle-aged Italians are. Oh, wait...
EXERCISE: When I was a lad, I used to run around in the street & playground like other kids. I was still fat. Exercise cannot compensate for poor diet (I ate lots of chocolate, cake & drank sugary Corona lemonade).
Why do we have to eat what farmers grow? Maybe if more people ate less powdered wheat products and more old-fashioned sourdough rye bread, farmers might start growing something else. There are plenty of carbohydrates that don't seriously disturb blood glucose levels, such as rice, rye, barley, quinoa, sorghum, millet, maize, sago, tubers, root veggies, bulbs, legumes & fresh whole fruits.
Nah, it'll never happen! Not while a) crap foods are dirt cheap and b) people keep following the dietary advice of "experts" like sheep ... or should that be lemmings?
See also Anthony Colpo's The Whole Grain Scam.
Sunday, 7 March 2010
Whatever happened to...Dr. A?
She left a comment on my previous blog post on 4th March. I posted a link to one of her blog posts on 5th March and the blog was not found. Her profile is not available and her main site's domain name has now expired.
This calls for some sombre music, until her return.
This calls for some sombre music, until her return.
Thursday, 4 March 2010
Coffee and brrrup-brrrap!
For those who have no idea what the title means, see Memorable quotes for How to Murder Your Wife (1965)
When I woke up this morning, I felt a bit "blech". I wasn't coming down with anything nasty. I just drank too much coffee yesterday! Coffee contains caffeine , which is a Central Nervous System stimulant. This gives you a brrrup (extra alertness & energy).
Sadly, what goes up eventually comes down, giving you a brrrap (feeling like crap, headachey).
Here's some soothing music for those of you who are "coming down" from caffeine or any other stimulant.
When I woke up this morning, I felt a bit "blech". I wasn't coming down with anything nasty. I just drank too much coffee yesterday! Coffee contains caffeine , which is a Central Nervous System stimulant. This gives you a brrrup (extra alertness & energy).
Sadly, what goes up eventually comes down, giving you a brrrap (feeling like crap, headachey).
Here's some soothing music for those of you who are "coming down" from caffeine or any other stimulant.
Sunday, 28 February 2010
We are not all the same.
Cont'd from Everyone is Different.
Lyle (McDonald) brought the following study to my attention to illustrate that "We are not all the same":- Some Metabolic Changes Induced by Low Carbohydrate Diets. On a very-low-carb diet, one subject’s total cholesterol rose to 12.9mmol/L (500mg/dL in US units). The others didn't.
See also LDL cholesterol goes sky high on fatty diet.
I posted the study in various blogs to make the above point. Here are some of the replies I got:-
"Lyle? Lyle McDonald? Is that where you got that study, Nigel?" and... "I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job."
"That was a weird study (1967) what I could make of it." and... "The men did all the stages but the women only did 3 stages of the diet."
"The fats were mostly omega-6 PUFA 13-35 grams worth..."
"The report you cite is so old and out of date that it makes me cry..."
My point was well & truly missed. I got the distinct impression that people thought I was criticising very-low-carb, high-fat diets. I wasn't. The simple fact is that there is no "One True Diet" that suits absolutely everybody. In the olden days everywhere & in poor countries nowadays, people that ate/eat the wrong diet for their body died/die young. Nowadays in rich countries, they get put on drugs e.g. oral hypoglycaemics (to lower blood glucose) & hypolipidaemics (to lower blood cholesterol/triglycerides).
Please note that omega-6 PUFAs tend to lower serum cholesterol rather than raise it, as per Figure. 1 below from Individual fatty acid effects on plasma lipids and lipoproteins: human studies.
However, don't rush off and eat shed-loads of omega-6 PUFA (e.g. corn oil) in the mistaken belief that it will make you live any longer.
Cont'd on Everyone is Different, Part 2.
Lyle (McDonald) brought the following study to my attention to illustrate that "We are not all the same":- Some Metabolic Changes Induced by Low Carbohydrate Diets. On a very-low-carb diet, one subject’s total cholesterol rose to 12.9mmol/L (500mg/dL in US units). The others didn't.
See also LDL cholesterol goes sky high on fatty diet.
I posted the study in various blogs to make the above point. Here are some of the replies I got:-
"Lyle? Lyle McDonald? Is that where you got that study, Nigel?" and... "I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job."
"That was a weird study (1967) what I could make of it." and... "The men did all the stages but the women only did 3 stages of the diet."
"The fats were mostly omega-6 PUFA 13-35 grams worth..."
"The report you cite is so old and out of date that it makes me cry..."
My point was well & truly missed. I got the distinct impression that people thought I was criticising very-low-carb, high-fat diets. I wasn't. The simple fact is that there is no "One True Diet" that suits absolutely everybody. In the olden days everywhere & in poor countries nowadays, people that ate/eat the wrong diet for their body died/die young. Nowadays in rich countries, they get put on drugs e.g. oral hypoglycaemics (to lower blood glucose) & hypolipidaemics (to lower blood cholesterol/triglycerides).
Please note that omega-6 PUFAs tend to lower serum cholesterol rather than raise it, as per Figure. 1 below from Individual fatty acid effects on plasma lipids and lipoproteins: human studies.
However, don't rush off and eat shed-loads of omega-6 PUFA (e.g. corn oil) in the mistaken belief that it will make you live any longer.
Cont'd on Everyone is Different, Part 2.
Tuesday, 23 February 2010
Things that make you go pink.
Strenuous exercise. Alcohol. High-dose Niacin. All of these things make you go pink. All of these things are also good for your heart & circulation. As I mentioned in Red, red wine and very sharp pointy things, one glass of red wine significantly lowered my blood pressure in less than 10 minutes, probably by making my arteries dilate (which made me go pink) and by reducing my mental stress which lowered my stress hormone levels.
According to JBS2 guidelines (which I don't fully agree with), CVD risk factor increases with increasing blood pressure. It also increases with increasing TC:HDL ratio. What increases HDL? Things that make you go pink. What we now need is a study showing the effects of blushing on the risk factors for CVD!
According to JBS2 guidelines (which I don't fully agree with), CVD risk factor increases with increasing blood pressure. It also increases with increasing TC:HDL ratio. What increases HDL? Things that make you go pink. What we now need is a study showing the effects of blushing on the risk factors for CVD!
Sunday, 21 February 2010
Natural & synthetic disaccharides.
As mentioned in Carbohydrates: Dogs' Doodads or Spawn of Satan?, there are three common disaccharides, sucrose (table sugar), lactose (milk sugar) and maltose (beer sugar). These all contain a molecule of glucose linked by a glycosidic bond to molecules of fructose, galactose and glucose respectively. In our bodies, our guts contain the enzymes sucrase, lactase & maltase which hydrolyse the glycosidic bond breaking the disaccharides into their constituent monosaccharides. People who lack any of these enzymes are unable to break the disaccharide into monosaccharides. As disaccharides are not absorbed, they pass along the gut until they reach the colon, where colonic bacteria ferment the disaccharides into short-chain fatty acids and gas. This increases ammonia levels in the colon which attracts water. End result: Lots of gas, soft poo and the excretion of ammonia (nitrogenous waste).
There's a synthetic disaccharide called lactulose, which is a disaccharide of fructose and galactose. As our bodies don't contain the enzyme lactulase, lactulose is fermented, producing lots of gas & soft poo. I thought I'd post about this as I'm taking lactulose to prevent the constipation caused by high dose Co-Codamol, the pain-killer I'm on while my 4-inch scar heals. It works!
An interesting but otherwise useless fact: The artificial sweetener sucralose that's made from & is about 600 times sweeter than sugar has the chemical name 1,6-Dichloro-1,6-dideoxy-β-D-fructofuranosyl-4-chloro-4-deoxy-α-D-galactopyranoside (I'm nerdy enough to know that by heart!). Sucralose has a structure like lactulose rather than sucrose, which has the chemical name β-D-fructofuranosyl-(2→1)-α-D-glucopyranoside. As the amount of sucralose used is about one 600th that of sucrose, it doesn't cause the above effects.
There's a synthetic disaccharide called lactulose, which is a disaccharide of fructose and galactose. As our bodies don't contain the enzyme lactulase, lactulose is fermented, producing lots of gas & soft poo. I thought I'd post about this as I'm taking lactulose to prevent the constipation caused by high dose Co-Codamol, the pain-killer I'm on while my 4-inch scar heals. It works!
An interesting but otherwise useless fact: The artificial sweetener sucralose that's made from & is about 600 times sweeter than sugar has the chemical name 1,6-Dichloro-1,6-dideoxy-β-D-fructofuranosyl-4-chloro-4-deoxy-α-D-galactopyranoside (I'm nerdy enough to know that by heart!). Sucralose has a structure like lactulose rather than sucrose, which has the chemical name β-D-fructofuranosyl-(2→1)-α-D-glucopyranoside. As the amount of sucralose used is about one 600th that of sucrose, it doesn't cause the above effects.
Wednesday, 17 February 2010
Red, red wine and very sharp pointy things.
Suffice it to say that I've been feeling a bit stressed recently, what with all the hoo-ha over my mum's nursing home etc. Today, I'm going to be prodded & cut open with very sharp pointy things as I'm having a right inguinal hernia repaired with polypropylene mesh.
Last Wednesday, I attended the pre-op' assessment and failed with a BP of 154/100. I explained that I had a very important meeting with Social Services on my mind and it was causing me much stress so I was told to get a re-test at my local surgery on Friday. As the meeting on Thursday didn't go quite as I'd hoped (case closed), my BP on Friday was 160/100. My GP upped my Amias dose from 8mg/day to 12mg/day and told me to get a re-test on Monday. I had to get my diastolic reading (the lower of the two numbers) below 90 or my op' would not take place today.
On Monday morning I tested my BP at home using my £9.99 Lloyds Pharmacy automatic BP meter (which usually gives the same reading as my GP's sphygmomanometer) and the lowest reading I could get was 135/99. Uh-oh! Desperate times call for desperate measures.
I hardly ever drink alcohol, but I had a bottle of Blossom Hill Californian Red in the cupboard for *ahem* special occasions, so I had a 250mL glass of it on an empty stomach. Woo-hoo! It went straight to my head and I felt slightly flushed. Ten minutes later, I was in the doctor's surgery having my BP tested. It was 140/86. Result! I told my GP what I'd done and he was O.K. with it. So, red wine for the win!
Before you all rush off and get hammered, here's an article from the Harvard School of Public Health about Alcohol: Balancing Risks and Benefits. The article used to contain a graph but it's been edited-out in the latest version. Luckily, I had a copy of it on my hard disk which I shall upload here.
As women have smaller livers than men, the cirrhosis graph shoots up faster for women as alcohol consumption increases beyond 1 drink per day.
Last Wednesday, I attended the pre-op' assessment and failed with a BP of 154/100. I explained that I had a very important meeting with Social Services on my mind and it was causing me much stress so I was told to get a re-test at my local surgery on Friday. As the meeting on Thursday didn't go quite as I'd hoped (case closed), my BP on Friday was 160/100. My GP upped my Amias dose from 8mg/day to 12mg/day and told me to get a re-test on Monday. I had to get my diastolic reading (the lower of the two numbers) below 90 or my op' would not take place today.
On Monday morning I tested my BP at home using my £9.99 Lloyds Pharmacy automatic BP meter (which usually gives the same reading as my GP's sphygmomanometer) and the lowest reading I could get was 135/99. Uh-oh! Desperate times call for desperate measures.
I hardly ever drink alcohol, but I had a bottle of Blossom Hill Californian Red in the cupboard for *ahem* special occasions, so I had a 250mL glass of it on an empty stomach. Woo-hoo! It went straight to my head and I felt slightly flushed. Ten minutes later, I was in the doctor's surgery having my BP tested. It was 140/86. Result! I told my GP what I'd done and he was O.K. with it. So, red wine for the win!
Before you all rush off and get hammered, here's an article from the Harvard School of Public Health about Alcohol: Balancing Risks and Benefits. The article used to contain a graph but it's been edited-out in the latest version. Luckily, I had a copy of it on my hard disk which I shall upload here.
As women have smaller livers than men, the cirrhosis graph shoots up faster for women as alcohol consumption increases beyond 1 drink per day.
Saturday, 13 February 2010
The problem with "Wholegrain" cereals etc.
As I mentioned in Carbohydrates: Dogs' Doodads or Spawn of Satan?, some breakfast cereals turn into blood glucose faster than table sugar (half glucose bonded with half fructose) even though they're "Wholegrain" cereals.
A whole (i.e. intact) grain consists of a protective outer shell (a.k.a. bran) and innards consisting of starchy/proteiny endosperm and nutritious germ. See Cereal germ.
To turn a grain into a breakfast cereal, it's milled into dust, mixed with water to form a paste and the paste is extruded through holes into whatever shape the manufacturer desires. Technically, everything that was in the whole grain is in the finished product. However, the form and function have completely changed. Here are a couple of analogies.
1) I want to sell my car. I take it to a scrap-yard and have it shredded into tiny pieces. All of the tiny pieces are put in a skip, which is delivered to my driveway. I place a sign on the skip stating "Whole Mazda MX-5 for sale. Enquire within. £5,000 O.N.O.". What would you offer for my "Whole Car"?
2) An insane person gives me £5,000 (in £50 notes) for my "Whole Car". As I'm on a roll, I take the notes and put them through a cross-cut shredder which turns them into thousands of 2mm x 2mm pieces. I empty the pieces into an attaché case. Who will accept my attaché case full of "Whole £50 notes" as payment for their second-hand car? Any more insane people out there?
Roller-milling grains into fine dust does four things.
1) It exposes the starchy endosperm.
2) It greatly increases the surface area to volume ratio of the grain, resulting in faster digestion and absorption. Surface area to volume ratio is inversely proportional to particle size. If 3mm grains are roller-milled into 0.1mm particles, the surface area to volume ratio is 30 times bigger. See Particle size, satiety and the glycaemic response. Therefore, "wholegrain" breads made from roller-milled flours are as bad as white breads, in terms of glucose and insulin response. Choose wholemeal breads made from stone-ground flours, as the particle size is bigger.
3) It makes the finished product much more likely to stick to your teeth, resulting in the rapid formation of plaque that damages your teeth and gums.
4) It makes the finished product more energy-dense.
Rolled grains are grains that have been steamed (to cook and make them soft), then put through what's effectively a mangle. They're still intact, if somewhat flat. Puffed grains are grains that have been heated to make the water within boil. As steam takes up a much larger volume than water, the grains are inflated to a much larger size. They're still intact, if somewhat funky-looking!
Don't be conned by breakfast cereal labels. If they look like "O"s or Brillo pads or brake pads, they're not intact grains.
Oats are O.K. even when turned into oatmeal, probably due to their high beta-glucan content, which forms a wallpaper paste-like goo when wet. See Particle size of wheat, maize, and oat test meals: effects on plasma glucose and insulin responses and on the rate of starch digestion in vitro.
See also Anthony Colpo's The Wholegrain Scam.
A whole (i.e. intact) grain consists of a protective outer shell (a.k.a. bran) and innards consisting of starchy/proteiny endosperm and nutritious germ. See Cereal germ.
To turn a grain into a breakfast cereal, it's milled into dust, mixed with water to form a paste and the paste is extruded through holes into whatever shape the manufacturer desires. Technically, everything that was in the whole grain is in the finished product. However, the form and function have completely changed. Here are a couple of analogies.
1) I want to sell my car. I take it to a scrap-yard and have it shredded into tiny pieces. All of the tiny pieces are put in a skip, which is delivered to my driveway. I place a sign on the skip stating "Whole Mazda MX-5 for sale. Enquire within. £5,000 O.N.O.". What would you offer for my "Whole Car"?
2) An insane person gives me £5,000 (in £50 notes) for my "Whole Car". As I'm on a roll, I take the notes and put them through a cross-cut shredder which turns them into thousands of 2mm x 2mm pieces. I empty the pieces into an attaché case. Who will accept my attaché case full of "Whole £50 notes" as payment for their second-hand car? Any more insane people out there?
Roller-milling grains into fine dust does four things.
1) It exposes the starchy endosperm.
2) It greatly increases the surface area to volume ratio of the grain, resulting in faster digestion and absorption. Surface area to volume ratio is inversely proportional to particle size. If 3mm grains are roller-milled into 0.1mm particles, the surface area to volume ratio is 30 times bigger. See Particle size, satiety and the glycaemic response. Therefore, "wholegrain" breads made from roller-milled flours are as bad as white breads, in terms of glucose and insulin response. Choose wholemeal breads made from stone-ground flours, as the particle size is bigger.
3) It makes the finished product much more likely to stick to your teeth, resulting in the rapid formation of plaque that damages your teeth and gums.
4) It makes the finished product more energy-dense.
Rolled grains are grains that have been steamed (to cook and make them soft), then put through what's effectively a mangle. They're still intact, if somewhat flat. Puffed grains are grains that have been heated to make the water within boil. As steam takes up a much larger volume than water, the grains are inflated to a much larger size. They're still intact, if somewhat funky-looking!
Don't be conned by breakfast cereal labels. If they look like "O"s or Brillo pads or brake pads, they're not intact grains.
Oats are O.K. even when turned into oatmeal, probably due to their high beta-glucan content, which forms a wallpaper paste-like goo when wet. See Particle size of wheat, maize, and oat test meals: effects on plasma glucose and insulin responses and on the rate of starch digestion in vitro.
See also Anthony Colpo's The Wholegrain Scam.
Tuesday, 9 February 2010
The problem with Diabetes.
Referring to Blood Glucose, Insulin & Diabetes, a healthy person regulates his/her blood glucose level so that it doesn't go too high or too low.
Someone who has diabetes either has insufficient/no insulin secretion (type 1) or has insulin secretion but it's ineffective (type 2). People with type 1 diabetes have to inject various types of insulin and monitor their Blood Glucose (BG) with a BG meter. Here lies the problem. Consider the following analogy:-
Blood glucose control is like driving down a road cut into the side of a mountain. If you steer too far to the left (low blood glucose), you fall off the edge of the road and die. If you steer too far to the right (high blood glucose), you smash yourself against the side of the mountain and damage yourself. Injecting insulin/taking oral hypoglycaemic agents is like pulling on the steering wheel to the left. Eating sugary/starchy carbs is like pulling on the steering wheel to the right. Exercising is like pulling on the steering wheel to the left.
Not monitoring BG regularly is like driving down the above road with your eyes shut most of the time. You have no idea where you are on the road. Every time you monitor BG, you open your eyes.
A high-glycaemic load diet + high-medication regimen (e.g. ADA & Diabetes-UK) is like pulling on the steering wheel hard, which results in diabetics veering all over the road. As diabetics don't want to fall off the edge of the road and die, they steer too far to the right (high average blood glucose) and damage themselves due to glycation.
A low-glycaemic load diet + low-medication regimen (e.g. Bernstein, Christie, Ruhl, Cooksey, Shwarzbein etc) is like pulling on the steering wheel gently, which results in diabetics steering a reasonably straight course down the middle of the road. Regular BG monitoring allows rapid error-correction.
As low blood glucose is potentially fatal, that's why Studies show that a high average blood glucose level has lower mortality than a more normal average blood glucose level.
Someone who has diabetes either has insufficient/no insulin secretion (type 1) or has insulin secretion but it's ineffective (type 2). People with type 1 diabetes have to inject various types of insulin and monitor their Blood Glucose (BG) with a BG meter. Here lies the problem. Consider the following analogy:-
Blood glucose control is like driving down a road cut into the side of a mountain. If you steer too far to the left (low blood glucose), you fall off the edge of the road and die. If you steer too far to the right (high blood glucose), you smash yourself against the side of the mountain and damage yourself. Injecting insulin/taking oral hypoglycaemic agents is like pulling on the steering wheel to the left. Eating sugary/starchy carbs is like pulling on the steering wheel to the right. Exercising is like pulling on the steering wheel to the left.
Not monitoring BG regularly is like driving down the above road with your eyes shut most of the time. You have no idea where you are on the road. Every time you monitor BG, you open your eyes.
A high-glycaemic load diet + high-medication regimen (e.g. ADA & Diabetes-UK) is like pulling on the steering wheel hard, which results in diabetics veering all over the road. As diabetics don't want to fall off the edge of the road and die, they steer too far to the right (high average blood glucose) and damage themselves due to glycation.
A low-glycaemic load diet + low-medication regimen (e.g. Bernstein, Christie, Ruhl, Cooksey, Shwarzbein etc) is like pulling on the steering wheel gently, which results in diabetics steering a reasonably straight course down the middle of the road. Regular BG monitoring allows rapid error-correction.
As low blood glucose is potentially fatal, that's why Studies show that a high average blood glucose level has lower mortality than a more normal average blood glucose level.
Monday, 8 February 2010
The problem with BMI.
According to my Body Mass Index, I'm just obese. The word "obese" conjures-up images of people with huge fat bellies waddling along. Sure I'm overweight as I love my food, but I don't have a huge fat belly and I don't waddle! The problem with BMI is that it's a simple calculation involving body mass and height.
BMI = body mass (in kg) divided by the square of height (in metres).
I will now demonstrate how two people with identical body compositions, waist measurements and heights can have different body masses (and thus BMIs). Consider the body as a cylinder with the legs as two inverted cones each having half the diameter of the body at the top (it keeps the maths relatively simple). I will ignore the arms & head!
Volume of a cylinder = Pi x Radius squared x Length.
Volume of a cone = 1/3 x Pi x Radius squared x Length.
Mass = Volume x Density.
Length of legs + body = 160cm.
Body diameter = 30cm.
Therefore, body radius = 15cm.
Leg diameter at top = 15cm.
Therefore, leg radius at top = 7.5cm.
Leg & body density = 1g/cubic centimetre.
I have 75cm long legs + 85cm long body.
She has 100cm long legs + 60cm long body.
My legs = 4420g each. My body = 60082g. My total body mass = 68922g = 69kg. My height = 1.6m.
∴ My BMI = 26.9
Her legs = 5900g each. Her body = 42411g. Her total body mass = 54211g = 54kg. Her height = 1.6m.
∴ Her BMI = 21.1
See the difference? 1cm of legs weighs much less than 1cm of body. People with long legs and a short body (e.g. women) have a significantly lower BMI than people with short legs and a long body (e.g. me). In addition, people with narrow builds and people with very little muscle have a significantly lower BMI than people with wide builds and people with a lot of muscle.
Thanks to Wolfram Alpha for doing the calculations.
P.S. According to her BMI, this 5 year old girl is overweight.
BMI = body mass (in kg) divided by the square of height (in metres).
I will now demonstrate how two people with identical body compositions, waist measurements and heights can have different body masses (and thus BMIs). Consider the body as a cylinder with the legs as two inverted cones each having half the diameter of the body at the top (it keeps the maths relatively simple). I will ignore the arms & head!
Volume of a cylinder = Pi x Radius squared x Length.
Volume of a cone = 1/3 x Pi x Radius squared x Length.
Mass = Volume x Density.
Length of legs + body = 160cm.
Body diameter = 30cm.
Therefore, body radius = 15cm.
Leg diameter at top = 15cm.
Therefore, leg radius at top = 7.5cm.
Leg & body density = 1g/cubic centimetre.
I have 75cm long legs + 85cm long body.
She has 100cm long legs + 60cm long body.
My legs = 4420g each. My body = 60082g. My total body mass = 68922g = 69kg. My height = 1.6m.
∴ My BMI = 26.9
Her legs = 5900g each. Her body = 42411g. Her total body mass = 54211g = 54kg. Her height = 1.6m.
∴ Her BMI = 21.1
See the difference? 1cm of legs weighs much less than 1cm of body. People with long legs and a short body (e.g. women) have a significantly lower BMI than people with short legs and a long body (e.g. me). In addition, people with narrow builds and people with very little muscle have a significantly lower BMI than people with wide builds and people with a lot of muscle.
Thanks to Wolfram Alpha for doing the calculations.
P.S. According to her BMI, this 5 year old girl is overweight.
Sunday, 7 February 2010
*Biff!* *Thwack!* *Ker-Pow!*
The Internet is a great place for a virtual punch-up. Nobody gets physically hurt (feelings can get very hurt!) and the end result is often educational as well as entertaining. Such a punch-up has just occurred between Alan Aragon (who's in my blog list) and Robert H. Lustig, M.D. (whose video is linked to in An apple a day...) plus quite a few others, including me.
Alan's blog post The bitter truth about fructose alarmism has caused a bit of a stir in the nutritional blogosphere.
Dr Lustig pointed out that lots of people have watched his video. If only Alan had some videos. Oh, wait! He has. They're in Conversations with a bro: animated edition. Also, see Alan Aragon on Paleo Cream Puffs and Is_Fructose_causing_problems_and_is_pointing_this_out_Alarmism_.mp4
Enjoy!
Alan's blog post The bitter truth about fructose alarmism has caused a bit of a stir in the nutritional blogosphere.
Dr Lustig pointed out that lots of people have watched his video. If only Alan had some videos. Oh, wait! He has. They're in Conversations with a bro: animated edition. Also, see Alan Aragon on Paleo Cream Puffs and Is_Fructose_causing_problems_and_is_pointing_this_out_Alarmism_.mp4
Enjoy!
Wednesday, 3 February 2010
A slight hitch, Part 2.
Continued from A slight hitch. It was on Friday February 13th 2009 that mum collapsed with a UTI and ended up in a nursing home after 3 weeks in hospital. As it had a 3-star CSCI (now CQC) rating, I thought that life would improve for her. Boy, was I wrong!
Due to me being depressed for about 6 months, I didn't deal with the endless litany of problems that mum's friend reported to me other than pass them on the the Home Manager for action. As there was no other nursing homes in the area that had a 3-star rating, both mum & I were stuck between a rock and a hard place.
Luckily, I broke out of the vicious circle of depression, crap diet, more depression, more crap diet etc. Then I saw the BBC documentary about Sir Gerry Robinson trying to "fix" dementia care homes. It wasn't just an eye-opener to Sir Gerry. It was an eye-opener to me, too. The programme showed me the difference between good nursing homes and crap nursing homes. Sadly, the nursing home that mum was in fell into the "crap" category, despite charging over £800 per week. I can't name names as I don't want to be sued.
I started to complain more vocally about the poor standard of care at mum's home but things weren't getting any better. One day, I bumped into the activities co-ordinator who was looking glum so I asked her what the matter was. She told me that she was leaving as she couldn't stand working there any more. I asked her what work she would be doing after leaving and she told me that she would be working as activities co-ordinator in a new nursing home that hadn't yet opened. I got the details off her and I was round there like a shot!
The upshot is that I am moving mum to the new nursing home when they are able to take her. In the meantime, I got the mobile number of an MD of the company that runs mum's current nursing home and complained to her. I had a meeting with the MD and two Operations managers and I thought that things would improve. Boy, was I wrong!
After yet more complaints from mum's friend and finding that the MD was on holiday, I reached the end of my tether and sent a complaint to the CQC, who contacted the Home Manager, who almost certainly contacted head office. I got an e-mail from the Senior Operations manager inviting me to another meeting, where I was metaphorically savaged for being "aggressive" and "intimidating" to staff at the nursing home. I am as aggressive and intimidating as a dead sheep! The next point will be of interest to anyone that has Power of Attorney.
Not a lot of people know this (myself included), but Enduring Power of Attorney gives you the authority to act on someone's behalf for property and financial affairs ONLY. I had no authority over mum's personal welfare and so all of the supplements that I had put her on to help her mental function were stopped pending investigation by an NHS dietician despite mum's GP O.K.'ing me to supply them.
The only way that I can have authority over mum's personal welfare is to become her Deputy, which means applying to the Court of Protection. COP1, COP1B, COP2, COP3 & COP4 are the relevant forms, plus COP44A as I would apply for fee exemption on the grounds of low income.
I also have to register my Enduring Power of Attorney with the Office of the Public Guardian, as mum's mental faculties are such that she can no longer make important decisions for herself. You need the Enduring Power of Attorney registration pack (ZIP 0.94MB).
I also contacted the Social Services Access Team to report mum as a vulnerable person at risk. There's going to be a "robust" meeting next week.
Continued on A slight hitch, Part 3.
Due to me being depressed for about 6 months, I didn't deal with the endless litany of problems that mum's friend reported to me other than pass them on the the Home Manager for action. As there was no other nursing homes in the area that had a 3-star rating, both mum & I were stuck between a rock and a hard place.
Luckily, I broke out of the vicious circle of depression, crap diet, more depression, more crap diet etc. Then I saw the BBC documentary about Sir Gerry Robinson trying to "fix" dementia care homes. It wasn't just an eye-opener to Sir Gerry. It was an eye-opener to me, too. The programme showed me the difference between good nursing homes and crap nursing homes. Sadly, the nursing home that mum was in fell into the "crap" category, despite charging over £800 per week. I can't name names as I don't want to be sued.
I started to complain more vocally about the poor standard of care at mum's home but things weren't getting any better. One day, I bumped into the activities co-ordinator who was looking glum so I asked her what the matter was. She told me that she was leaving as she couldn't stand working there any more. I asked her what work she would be doing after leaving and she told me that she would be working as activities co-ordinator in a new nursing home that hadn't yet opened. I got the details off her and I was round there like a shot!
The upshot is that I am moving mum to the new nursing home when they are able to take her. In the meantime, I got the mobile number of an MD of the company that runs mum's current nursing home and complained to her. I had a meeting with the MD and two Operations managers and I thought that things would improve. Boy, was I wrong!
After yet more complaints from mum's friend and finding that the MD was on holiday, I reached the end of my tether and sent a complaint to the CQC, who contacted the Home Manager, who almost certainly contacted head office. I got an e-mail from the Senior Operations manager inviting me to another meeting, where I was metaphorically savaged for being "aggressive" and "intimidating" to staff at the nursing home. I am as aggressive and intimidating as a dead sheep! The next point will be of interest to anyone that has Power of Attorney.
Not a lot of people know this (myself included), but Enduring Power of Attorney gives you the authority to act on someone's behalf for property and financial affairs ONLY. I had no authority over mum's personal welfare and so all of the supplements that I had put her on to help her mental function were stopped pending investigation by an NHS dietician despite mum's GP O.K.'ing me to supply them.
The only way that I can have authority over mum's personal welfare is to become her Deputy, which means applying to the Court of Protection. COP1, COP1B, COP2, COP3 & COP4 are the relevant forms, plus COP44A as I would apply for fee exemption on the grounds of low income.
I also have to register my Enduring Power of Attorney with the Office of the Public Guardian, as mum's mental faculties are such that she can no longer make important decisions for herself. You need the Enduring Power of Attorney registration pack (ZIP 0.94MB).
I also contacted the Social Services Access Team to report mum as a vulnerable person at risk. There's going to be a "robust" meeting next week.
Continued on A slight hitch, Part 3.
Saturday, 30 January 2010
Good Science: Doubly-labeled water
I was reading an interview with Rudolph L. Leibel and doubly-labeled water was mentioned. This sort of stuff fascinates me. Using doubly-labeled water, a mass spectrometer, loads of measurements and some mathematics, it's possible to work out how many kcals someone is burning. This method costs an arm & a leg. So, how does doubly-labeled water work?
Chemistry 101:
Water has the formula H2O. H stands for Hydrogen and O stands for Oxygen.
Elements have isotopes. Hydrogen has two isotopes, Deuterium and Tritium. Deuterium oxide, or D2O is known as heavy water and one use for heavy water is the manufacture of atomic bombs, if you recall the film "The heroes of Telemark". Deuterium is non-radioactive, as is heavy water. Tritium is radioactive.
Oxygen has three stable non-radioactive isotopes one of which is O-18. This can be used to make labeled water H2O-18. Mix D2O with a bit of H2O-18 and you have doubly-labeled water. Now what? To quote Leibel:-
"The interesting thing is that when you give somebody water like this, the deuterium comes out of the body which is determined by water turnover in the individual. The O-18 is in equilibrium with carbon dioxide, so the O-18 comes out by two mechanisms: first with normal water by transpiration, perspiration and urine, but also in the breath.
The difference between those two decay curves (the O-18 comes out faster), which we obtain by getting urine from these patients every day for 10 days-that gap is proportional to carbon dioxide production in that individual. By doing this, we can figure out how much carbon dioxide this person made over a period of 10 days. Knowing that, and knowing what the so-called diet quotient is - in other words, what the ratio of carbohydrates to fat in their diet is - you can back-calculate the amount of oxygen used to produce that amount of carbon dioxide.
So by some simple algebra using the rate of carbon dioxide excretion, you can actually calculate how much oxygen their body used in the process of oxidative metabolism. That is a very critical number because it tells you how much energy they burned. Oxygen consumption can be immediately converted into calories.
So we measure caloric expenditure both by figuring out how many calories it takes to make their body weight absolutely stable, and checking that number by also using this double-doped water excretion technique using mass spectroscopy. It's quite expensive: the isotopes to do such a study cost about $500, not including the spectroscopy."
See A comparative study of different means of assessing long-term energy expenditure in humans.
Ain't science wonderful?
Chemistry 101:
Water has the formula H2O. H stands for Hydrogen and O stands for Oxygen.
Elements have isotopes. Hydrogen has two isotopes, Deuterium and Tritium. Deuterium oxide, or D2O is known as heavy water and one use for heavy water is the manufacture of atomic bombs, if you recall the film "The heroes of Telemark". Deuterium is non-radioactive, as is heavy water. Tritium is radioactive.
Oxygen has three stable non-radioactive isotopes one of which is O-18. This can be used to make labeled water H2O-18. Mix D2O with a bit of H2O-18 and you have doubly-labeled water. Now what? To quote Leibel:-
"The interesting thing is that when you give somebody water like this, the deuterium comes out of the body which is determined by water turnover in the individual. The O-18 is in equilibrium with carbon dioxide, so the O-18 comes out by two mechanisms: first with normal water by transpiration, perspiration and urine, but also in the breath.
The difference between those two decay curves (the O-18 comes out faster), which we obtain by getting urine from these patients every day for 10 days-that gap is proportional to carbon dioxide production in that individual. By doing this, we can figure out how much carbon dioxide this person made over a period of 10 days. Knowing that, and knowing what the so-called diet quotient is - in other words, what the ratio of carbohydrates to fat in their diet is - you can back-calculate the amount of oxygen used to produce that amount of carbon dioxide.
So by some simple algebra using the rate of carbon dioxide excretion, you can actually calculate how much oxygen their body used in the process of oxidative metabolism. That is a very critical number because it tells you how much energy they burned. Oxygen consumption can be immediately converted into calories.
So we measure caloric expenditure both by figuring out how many calories it takes to make their body weight absolutely stable, and checking that number by also using this double-doped water excretion technique using mass spectroscopy. It's quite expensive: the isotopes to do such a study cost about $500, not including the spectroscopy."
See A comparative study of different means of assessing long-term energy expenditure in humans.
Ain't science wonderful?
Thursday, 28 January 2010
The key to happiness
AC-CENT-TCHU-ATE THE POSITIVE (Mister In-Between)
(Johnny Mercer/Harold Arlen, sung by Bing Crosby)
You've got to accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
You've got to spread joy up to the maximum
Bring gloom down to the minimum
Have faith or pandemonium
Liable to walk upon the scene
(To illustrate his last remark
Jonah in the whale, Noah in the ark
What did they do
Just when everything looked so dark)
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No, do not mess with Mister In-Between
Do you hear me, hmm?
(Oh, listen to me children and-a you will hear
About the elininatin' of the negative
And the accent on the positive)
And gather 'round me children if you're willin'
And sit tight while I start reviewin'
The attitude of doin' right
(You've gotta accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between)
You've got to spread joy (up to the maximum)
Bring gloom (down) down to the minimum
Otherwise (otherwise) pandemonium
Liable to walk upon the scene
To illustrate (well illustrate) my last remark (you got the floor)
Jonah in the whale, Noah in the ark
What did they say (what did they say)
Say when everything looked so dark
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No! Don't mess with Mister In-Between
(Johnny Mercer/Harold Arlen, sung by Bing Crosby)
You've got to accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
You've got to spread joy up to the maximum
Bring gloom down to the minimum
Have faith or pandemonium
Liable to walk upon the scene
(To illustrate his last remark
Jonah in the whale, Noah in the ark
What did they do
Just when everything looked so dark)
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No, do not mess with Mister In-Between
Do you hear me, hmm?
(Oh, listen to me children and-a you will hear
About the elininatin' of the negative
And the accent on the positive)
And gather 'round me children if you're willin'
And sit tight while I start reviewin'
The attitude of doin' right
(You've gotta accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between)
You've got to spread joy (up to the maximum)
Bring gloom (down) down to the minimum
Otherwise (otherwise) pandemonium
Liable to walk upon the scene
To illustrate (well illustrate) my last remark (you got the floor)
Jonah in the whale, Noah in the ark
What did they say (what did they say)
Say when everything looked so dark
Man, they said we better
Accentuate the positive
Eliminate the negative
Latch on to the affirmative
Don't mess with Mister In-Between
No! Don't mess with Mister In-Between
Wednesday, 27 January 2010
When good science goes bad
I was rummaging through PubMed (as you do) and it occurred to me that there's a problem.
1) The conclusions in the abstracts don't always tie-up with the data in the full studies.
2) There is no mention of who funded the studies.
3) There is no mention of any conflict of interest for the authors.
Some abstracts link to a free full study and some don't. This makes it difficult to know which studies have been "fixed" to achieve a desired outcome by tweaking the methodology. For example, here are some studies involving Hunter SJ, in chronological order:-
Elderly women in northern New England exhibit seasonal changes in bone mineral density and calciotropic hormones which is about seasonal variations in Vitamin D status affecting bone density and was co-authored by Michael Holick.
Demonstration of Glycated Insulin in Human Diabetic Plasma and Decreased Biological Activity Assessed by Euglycemic-Hyperinsulinemic Clamp Technique in Humans which is about how high blood glucose glycates insulin before it's even secreted, resulting in it working less well in muscle cells.
Reduced prevalence of limited joint mobility in type 1 diabetes in a U.K. clinic population over a 20-year period which pretty much does what it says on the tin.
Then, Hunter starts working for The Sugar Bureau and begins co-authoring studies like this:-
Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, scrutinised in Who pays the piper
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial, scrutinised in Who pays the piper part 2
and
Session 4: CVD, diabetes and cancer Diet, insulin resistance and diabetes: the right (pro)portions, which concludes "based on the results of diabetes prevention trials focusing on lifestyle measures, evidence favours low-fat diets as the preferred approach for weight loss and diabetes prevention."
Evidence favours low-fat diets for weight loss and diabetes prevention, huh? See Low-carb diet pitted against low-fat PLUS medication (low-carb still wins) and Diabetes Update
So, getting paid by an organisation which promotes the consumption of sugar makes good science go bad.
1) The conclusions in the abstracts don't always tie-up with the data in the full studies.
2) There is no mention of who funded the studies.
3) There is no mention of any conflict of interest for the authors.
Some abstracts link to a free full study and some don't. This makes it difficult to know which studies have been "fixed" to achieve a desired outcome by tweaking the methodology. For example, here are some studies involving Hunter SJ, in chronological order:-
Elderly women in northern New England exhibit seasonal changes in bone mineral density and calciotropic hormones which is about seasonal variations in Vitamin D status affecting bone density and was co-authored by Michael Holick.
Demonstration of Glycated Insulin in Human Diabetic Plasma and Decreased Biological Activity Assessed by Euglycemic-Hyperinsulinemic Clamp Technique in Humans which is about how high blood glucose glycates insulin before it's even secreted, resulting in it working less well in muscle cells.
Reduced prevalence of limited joint mobility in type 1 diabetes in a U.K. clinic population over a 20-year period which pretty much does what it says on the tin.
Then, Hunter starts working for The Sugar Bureau and begins co-authoring studies like this:-
Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial, scrutinised in Who pays the piper
Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial, scrutinised in Who pays the piper part 2
and
Session 4: CVD, diabetes and cancer Diet, insulin resistance and diabetes: the right (pro)portions, which concludes "based on the results of diabetes prevention trials focusing on lifestyle measures, evidence favours low-fat diets as the preferred approach for weight loss and diabetes prevention."
Evidence favours low-fat diets for weight loss and diabetes prevention, huh? See Low-carb diet pitted against low-fat PLUS medication (low-carb still wins) and Diabetes Update
So, getting paid by an organisation which promotes the consumption of sugar makes good science go bad.
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