Archive for October, 2013

CONSERVATIVES, GET YOUR STICKY NOSES OUT OF MY BUSINESS!!!

Posted in ONLINE DEBATE with tags , , , , , , , , , on October 30, 2013 by drjgelb

October 30, 2013 0116h

How myopic American conservatives seem to be! Conservatives directly oppose the overwhelming majority view on several key issues related to personal morality, gender, sexuality and choice. Whether it’s trying to limit reimbursement for birth-control in order to limit its reach, or opposing women’s right to control their own bodies, or insisting on maintaining Prohibition of illicit drugs contrary to most international experts, American conservatives do not listen or respect the American people and their wishes. Instead, conservatives think they know better and that their morality is the only acceptable variety. I must disappoint you all……in a country like Australia, only a tiny minority express agreement with your views. Abortion is freely available and assisted by Government, political parties have left the public bedroom and are increasingly minding their own business at last. Prostitution is legal and very well regulated and there is general acceptance of each person’s right to decide their values for themselves. American Conservatives want to take America back 50yrs before the next generation of enlightened young Americans assume power and legislate proscriptive statutes into history. What about your beloved constitution Conservatives? What about majority rules? What about equality for all? At least tell yourselves the truth…….that you want everyone to believe what you do and you reject anyone with a contrary view.

This post by Steve Straub of “The Federalist Papers” (http://www.thefederalistpapers.org/current-events/first-amendment-under-assault#comment-145620) laments progressive gains in the U.S. and is commented on by a range of hard right-wing zealots that appear to be in a moral panic about the American public living their lives as they wish.

“There appears to be a full on assault on the first amendment, Christians and conservatives within the military.

Todd Starnes from FOX News reports:

Soldiers attending a pre-deployment briefing at Fort Hood say they were told that evangelical Christians and members of the Tea Party were a threat to the nation and that any soldier donating to those groups would be subjected to punishment under the Uniform Code of Military Justice. A soldier who attended the Oct. 17th briefing told me the counter-intelligence agent in charge of the meeting spent nearly a half hour discussing how evangelical Christians and groups like the American Family Association were “tearing the country apart.” In my opinion the Obama administration is determined to transform the Armed Forces into a liberal/progressive institution by chasing out those opposed to their policy goals.”

My comment is expressed as politely as I can make it but I really feel like shaking Conservatives and telling them to fuck off and take their noses out of my business.

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VITAMIN D – DANGEROUSLY DEFICIENT!

Posted in PSYCHIATRY with tags , , , on October 21, 2013 by drjgelb

VITAMIN D DEFICIENCY IS THE UNDESIRABLE NEW NORM IN THE DIGITAL AGE, WITH DEVASTATING INCREASES IN EARLY ONSET OSTEOPOROSIS AND BONE FRACTURES AND LIKELY INVOLVEMENT IN DEPRESSION, DEMENTIA AND CANCER. MUCH WORK REMAINS TO BE DONE BUT THERE IS NO DOUBT THAT IF YOU WORK INDOORS, IT IS IMPOSSIBLE AND UNSAFE TO LIVE IN Melbourne AND GET SUFFICIENT UNPROTECTED MIDDLE OF THE DAY SUNLIGHT TO MAINTAIN VIT.D STORES WITHOUT SUPPLEMENTATION. AN INCREASING INCIDENCE OF RICKETTS IN CHIDREN OF DARK SKINNED MIGRANTS AND RATES OF DEFICIENCY IN PREGNANT VEILED WOMEN EXCEEDING 80%, MUST RING ALARM BELLS FOR HEALTH AUTHORITIES. PERHAPS IT’s TIME TO FINESSE THE SLIP, SLOP, SLAP MESSAGE WITH A SOFTER MESSAGE ABOUT SUN EXPOSURE OUTSIDE THE DANGEROUS 4-6hr MIDDLE OF THE DAY WINDOW. eg. Exposure until 10am and after 3pm requires less aggressive use of sun protection strategies

OR ARE PEOPLE TOO EASILY CONFUSED TO RISK IT?

ANYWAY, HERE ARE THE FACTS FYI:

VITAMIN D DEFICIENCY – WIDESPREAD AND MORE SERIOUS THAN PREVIOUSLY KNOWN!

The major function of Vitamin D in humans is to maintain appropriate serum calcium concentrations by enhancing the ability of the small intestine to absorb calcium from the diet. Vitamin D also plays a role in enhancing absorption of phosphorus from the diet, but the blood concentration of phosphorus is not well regulated and varies according to supply and the renal excretory threshold.

Vitamin D maintains the blood calcium at supersaturating levels such that it is deposited in the bone as calcium hydroxyapatite. When dietary calcium is inadequate for the body’s needs, 1,25-dihydroxyvitamin D [1,25(OH)2D or calcitriol] – the active form of vitamin D – together with parathyroid hormone, can mobilise stem cells in bone marrow to become mature osteoclasts which in turn increase the mobilisation of calcium stores from bone. However, there is a limited capacity to mobilise sufficient calcium from bone to have a significant effect on blood calcium levels.

Vitamin D occurs in two forms. One is produced by the action of sunlight on skin (D3 or cholecalciferol) and the other is found in a limited range of foods (D2 or ergocalciferol). With current food supplies and patterns of eating, it is almost impossible to obtain sufficient vitamin D from the diet alone (Fuller & Casparian 2001). Vitamin D in foods is fat soluble and is biologically less active. Its metabolite, 1.25-dihydroxyvitamin D (1,25(OH2)D, or calcitriol) is the biologically active hormone responsible for its physiological actions. In the circulation, vitamin D appears as 25-hydroxyvitamin D (25(OH)D) which is five times more potent than cholecalciferol.

Vitamin D status is generally maintained in the population by exposure to sunlight (Glerup et al 2000, Holick 1996, Rasmussen et al 2000). If sunlight exposure is adequate, dietary vitamin D can be considered unnecessary (Holick 2001). In skin, 7-dehydrocholesterol is converted to pre-vitamin D3 by a narrow band of solar ultraviolet radiation (290-320 nm) which undergoes isomerisation in a temperature-dependent manner to vitamin D3.

Thus, vitamin D is not a nutrient in the usual sense, since under normal conditions it is supplied mainly by the skin. In addition, its physiological actions are attributable to the active metabolite, 1,25-dihydroxyvitamin D which, because it is synthesised in the kidneys and acts elsewhere, is often called a hormone.

1 µg cholecalciferol is equal to 0.2 µg 25(OH)D. Vitamin D is also sometimes expressed in International Units where 1 IU equals 0.025 µg cholecalciferol or 0.005 µg 25(OH)D.

Seasonal changes have been shown to have a significant effect on the cutaneous production of cholecalciferol (Pettifor et al 1996, Webb et al 1990). In the winter months in temperate latitudes, solar UV light in the wavelength range of 290-320 nm is absorbed by the atmosphere. People also spend less time outdoors and wear more clothing. For this reason, vitamin D deficiency is more common in the winter months (Holick 1995).

Despite the sunny climate, a seasonal variation in vitamin D levels also occurs in Australia. In the Geelong Osteoporosis Study, the mean vitamin D levels for winter were 58 nmol/L compared with 70 nmol/L in summer (Pasco et al 2001). However, after regular sun exposure, people under the age of 50 can produce and store approximately 6 months’ worth of vitamin D, so vitamin D stored in the body is available during the winter when production is minimal (Holick 1996). However, in older people, the efficiency of cutaneous synthesis of vitamin D is significantly less than that in younger people (Holick et al 1989, Need et al 1993).

Other environmental factors such as the angle of the sun, distance from the equator, the amount of cloud cover and the amount of particulate matter in the atmosphere (Holick 1995, Kimlin et al 2003, Madronich et al 1998) can affect the amount of vitamin D produced. Comparative data indicate that Northern and Southern latitudes are not equivalent. It has been estimated that ultraviolet levels in summer are up to 40% higher in New Zealand than in the equivalent Northern latitudes (Madronich et al 1998).

Deficiency of Vitamin D results in inadequate mineralisation or demineralisation of the skeleton. This can lead to rickets in young children, causing bowed legs and knocked knees., A study in China showed that vitamin D given as a supplement over 2 years increased both total body bone mineral content and bone mineral density in older children (Du et al 2004). In adults, deficiency can lead to increased bone turnover and osteoporosis and less commonly to osteomalacia for which the associated secondary hyperparathyroidism enhances mobilisation of calcium from the skeleton, resulting in porotic bone. Vitamin D may also affect fracture rates via mechanisms other than its influence on bone mass. Bischoff-Ferrari et al (2004) showed that on the basis of five RCTs involving 1,237 participants, vitamin D reduced the number of falls by 22% compared with patients receiving calcium or placebo.

Vitamin D is also thought to play a role in maintaining the immune system (Brown et al1999, DeLuca 1998) and helping maintain healthy skin (DeLuca 1998, Jones et al 1998) and muscle strength (Brown et al 1999).

There is increasing recognition that a significant number of Australians and New Zealanders may have less than optimal 25(OH)D status, however limited published information of the prevalence of vitamin D deficiency in Australia is available, other than from relatively small subpopulations (Nowson & Margerison 2002, Pasco et al 2004). Some information is available currently in unpublished form, from the national surveys of 1997 and 2002 in New Zealand (Green et al 2004a,b). Recent analyses of blood samples from these surveys showed that 31% of New Zealand children aged 5-14years whose bloods were sampled in 2002 had a serum 25(OH)D concentration indicative of vitamin D insufficiency. Between 0% (for 5-6 year olds of European background) and 14% (for girls aged 11-14 years of Pacific Island backgrounds) had vitamin D deficiency. For adolescents at or above 15 years and adults whose bloods were sampled in 1997, the prevalence of deficiency, defined as <17.5 nmol/L, was 2.8%, but the prevalence of insufficiency, defined as 70 yr 15.0 µg /day
Women
19-30 yr 5.0 µg /day
31-50 yr 5.0 µg /day
51-70 yr 10.0 µg /day
>70 yr 15.0 µg /day
Rationale: The AI for younger adults (19-50 years) is based on the amount of vitamin D required to maintain serum 25(OH)D at a level of at least 27.5 nmol/L with minimal exposure to sunlight. One study of US women of this age (Kinyamu et al 1997) showed that an average intake of 3.3-3.4 µg/day resulted in serum 25(OH)D of greater than 30 nmol/L. A study of females in Australia undertaken across both the summer and winter months at latitude 38o (Pasco et al 2001), assessed median intakes to be only 1.3 µg/day (much lower than other estimates for Australia and New Zealand), but had only 7% of subjects with serum 25(OH)D below 28 nmol/L in summer and 11% in winter. A vitamin D intake of 2.5 µg/day was seen as prudent for this age group. There are no data on men on which to set a figure except from one study of submariners not exposed to sunlight, whose status was assessed with or without a 15 µg/day supplement (Holick, 1994). However, the effects of lower doses were not assessed in this study. It is therefore assumed that requirements for men will be the same as those for women.

To cover the needs of all adults in the age range of 19-50 years, regardless of exposure to sunlight and in recognition of the fact that the available data were collected in women, a figure of 5 µg/day was set as the AI for younger adults. The AI was raised to 10 µg/day for adults aged 51-70 years to account for the reduced capacity for the skin to produce vitamin D with ageing (Holick et al 1989, Need et al 1993). Data on bone loss and vitamin D supplementation in women were also taken into consideration (Dawson-Hughes et al 1991, 1995). For adults over 70 years, the AI was raised to 15 µg/day. Studies of elderly people with intakes of 9.6 µg, 7.1 µg or 5.2 µg vitamin D/day showed that 8, 14 and 45%, respectively had low levels of serum 25(OH)D (Gloth et al 1995, Kinyamu et al 1997, O’Dowd et al 1993). A value of 7.5 µg/day was considered prudent for those with limited sun exposure and was doubled to 15 µg/day to cover the needs of all adults of this age, regardless of sun exposure or body stores.

It should be noted that the effect of increasing the dietary intake of vitamin D on 25(OH)D concentration in blood varies according to the existing vitamin D status of the individual. The status of those with low 25(OH)D levels in plasma will be improved to a more significant degree than of those with pre-existing high status (eg plasma levels above about 50 nmol/L) who may benefit little from the additional dietary intake.

Role of sunlight exposure: There is evidence from selected subpopulations that about 4-8% of adults in Australia have serum 25(OH)D levels below 28 nmol/L and about 30% have levels below 50 nmol/L. (Pasco et al 2001, MacGrath et al 2001, Vasikaran et al 2000). National surveys in New Zealand have indicated that some 2.8% of adults have levels of less than 17.5 nmol/L and 27.6% have levels below 37.5 nmol/L. Both sunlight and diet play an essential role in vitamin D status in younger adults. Kimlin et al (2003) estimated that for an older woman with fair skin, exposure of 6% of the body surface (face, hands, forearm) to sunlight for 15-30 minutes, 2-3 times per week would provide the equivalent of 15 µg vitamin D/day. Because of reduced cutaneous production, young adults (19-50 years) who live in southern latitudes such as Tasmania and the southern island of New Zealand are particularly at risk of becoming vitamin D deficient during the winter months.

For dark-skinned peoples such as indigenous Australians and New Zealanders and certain migrant groups and veiled women, there is evidence in Australia of high rates of vitamin D deficiency. Grover et al (2001) found that 80% of pregnant dark-skinned, veiled women attending one antenatal clinic in a large teaching hospital had vitamin D levels of less than 22 nmol/L. For people with little access to sunlight a supplement of 10 µg/day would not be excessive.

Institutionalised elderly: Several studies in Australia and New Zealand have shown high rates of deficiency in very elderly people with restricted access to sunlight, many of whom live in institutions. Estimates of deficiency range from 15-52% in Australia (Bruce et al 1999, Flicker et al 2003, Inderjeeth et al 2000, Stein 1996). Ley et al (1999) found that 49% of older New Zealand subjects in winter and 33% in summer had low serum 25(OH)D while McAuley et al (1997) reported 69% of subjects in Dunedin having low levels in winter, but only 26% in summer. Data from the National Nutrition Survey of New Zealand (Green et al 2004b) showed that 1.6% of males over 65 years and 5.8% of females had blood levels below 17.5 nmol/L for serum 25(OH)D and that 20.5% of men and 39.6% of women had levels below 37.5 nmol/L. This survey did not include institutionalised people. The recommendation of 15 µg/day for those over 70 years relates to the general population over 70 years. A number of recent studies demonstrate protection from falls and fractures with supplemental intakes of vitamin D in the elderly.

For institutionalised or bed-bound elderly who have very restricted exposure to sunlight often accompanied by reduced food intake, supplementation with vitamin D in the order of 10-25 µg/day may be necessary (Brazier et al 1995, Byrne et al 1995, Chapuy et al 1992, Egsmose et al 1987, Fardellone et al 1995, Kamel et al 1996, McKenna 1992, Sebert et al 1995, Sorva et al 1991).

Pregnancy

Age AI
14-18 yr 5.0 µg/day
19-30 yr 5.0 µg/day
31-50 yr 5.0 µg/day
Rationale: Although there is placental transfer of vitamin D and its metabolites from mother to foetus, the amounts are too small to affect the mother’s vitamin D requirement, particularly as there is a rise in serum calcitriol (probably of placental origin) and a rise in calcium absorption in late pregnancy (Paunier et al 1978, Specker 2004). However, maternal deficiency of vitamin D can affect the foetus and needs to be prevented. Pregnant women who receive regular exposure to sunlight do not require supplementation. However, at intakes of less than 3.8 µg/day, pregnant women in winter months at high latitudes have been shown to have low serum 25(OH)D (Paunier et al 1978). For women who have little access to sunlight, a supplement of 10 µg/day prenatally would not be excessive. In the last trimester of pregnancy there is quite a large transfer of 25(OH)D across the placenta.

Vitamin D

Background

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The major function of Vitamin D in humans is to maintain appropriate serum calcium concentrations by enhancing the ability of the small intestine to absorb calcium from the diet. Vitamin D also plays a role in enhancing absorption of phosphorus from the diet, but the blood concentration of phosphorus is not well regulated and varies according to supply and the renal excretory threshold.

Vitamin D maintains the blood calcium at supersaturating levels such that it is deposited in the bone as calcium hydroxyapatite. When dietary calcium is inadequate for the body’s needs, 1,25-dihydroxyvitamin D [1,25(OH)2D or calcitriol] – the active form of vitamin D – together with parathyroid hormone, can mobilise stem cells in bone marrow to become mature osteoclasts which in turn increase the mobilisation of calcium stores from bone. However, there is a limited capacity to mobilise sufficient calcium from bone to have a significant effect on blood calcium levels.

Vitamin D occurs in two forms. One is produced by the action of sunlight on skin (D3 or cholecalciferol) and the other is found in a limited range of foods (D2 or ergocalciferol). With current food supplies and patterns of eating, it is almost impossible to obtain sufficient vitamin D from the diet alone (Fuller & Casparian 2001). Vitamin D in foods is fat soluble and is biologically less active. Its metabolite, 1.25-dihydroxyvitamin D (1,25(OH2)D, or calcitriol) is the biologically active hormone responsible for its physiological actions. In the circulation, vitamin D appears as 25-hydroxyvitamin D (25(OH)D) which is five times more potent than cholecalciferol.

Vitamin D status is generally maintained in the population by exposure to sunlight (Glerup et al 2000, Holick 1996, Rasmussen et al 2000). If sunlight exposure is adequate, dietary vitamin D can be considered unnecessary (Holick 2001). In skin, 7-dehydrocholesterol is converted to pre-vitamin D3 by a narrow band of solar ultraviolet radiation (290-320 nm) which undergoes isomerisation in a temperature-dependent manner to vitamin D3.

Thus, vitamin D is not a nutrient in the usual sense, since under normal conditions it is supplied mainly by the skin. In addition, its physiological actions are attributable to the active metabolite, 1,25-dihydroxyvitamin D which, because it is synthesised in the kidneys and acts elsewhere, is often called a hormone.

1 µg cholecalciferol is equal to 0.2 µg 25(OH)D. Vitamin D is also sometimes expressed in International Units where 1 IU equals 0.025 µg cholecalciferol or 0.005 µg 25(OH)D.

Seasonal changes have been shown to have a significant effect on the cutaneous production of cholecalciferol (Pettifor et al 1996, Webb et al 1990). In the winter months in temperate latitudes, solar UV light in the wavelength range of 290-320 nm is absorbed by the atmosphere. People also spend less time outdoors and wear more clothing. For this reason, vitamin D deficiency is more common in the winter months (Holick 1995).

Despite the sunny climate, a seasonal variation in vitamin D levels also occurs in Australia. In the Geelong Osteoporosis Study, the mean vitamin D levels for winter were 58 nmol/L compared with 70 nmol/L in summer (Pasco et al 2001). However, after regular sun exposure, people under the age of 50 can produce and store approximately 6 months’ worth of vitamin D, so vitamin D stored in the body is available during the winter when production is minimal (Holick 1996). However, in older people, the efficiency of cutaneous synthesis of vitamin D is significantly less than that in younger people (Holick et al 1989, Need et al 1993).

Other environmental factors such as the angle of the sun, distance from the equator, the amount of cloud cover and the amount of particulate matter in the atmosphere (Holick 1995, Kimlin et al 2003, Madronich et al 1998) can affect the amount of vitamin D produced. Comparative data indicate that Northern and Southern latitudes are not equivalent. It has been estimated that ultraviolet levels in summer are up to 40% higher in New Zealand than in the equivalent Northern latitudes (Madronich et al 1998).

Deficiency of Vitamin D results in inadequate mineralisation or demineralisation of the skeleton. This can lead to rickets in young children, causing bowed legs and knocked knees., A study in China showed that vitamin D given as a supplement over 2 years increased both total body bone mineral content and bone mineral density in older children (Du et al 2004). In adults, deficiency can lead to increased bone turnover and osteoporosis and less commonly to osteomalacia for which the associated secondary hyperparathyroidism enhances mobilisation of calcium from the skeleton, resulting in porotic bone. Vitamin D may also affect fracture rates via mechanisms other than its influence on bone mass. Bischoff-Ferrari et al (2004) showed that on the basis of five RCTs involving 1,237 participants, vitamin D reduced the number of falls by 22% compared with patients receiving calcium or placebo.

Vitamin D is also thought to play a role in maintaining the immune system (Brown et al1999, DeLuca 1998) and helping maintain healthy skin (DeLuca 1998, Jones et al 1998) and muscle strength (Brown et al 1999).

There is increasing recognition that a significant number of Australians and New Zealanders may have less than optimal 25(OH)D status, however limited published information of the prevalence of vitamin D deficiency in Australia is available, other than from relatively small subpopulations (Nowson & Margerison 2002, Pasco et al 2004). Some information is available currently in unpublished form, from the national surveys of 1997 and 2002 in New Zealand (Green et al 2004a,b). Recent analyses of blood samples from these surveys showed that 31% of New Zealand children aged 5-14years whose bloods were sampled in 2002 had a serum 25(OH)D concentration indicative of vitamin D insufficiency. Between 0% (for 5-6 year olds of European background) and 14% (for girls aged 11-14 years of Pacific Island backgrounds) had vitamin D deficiency. For adolescents at or above 15 years and adults whose bloods were sampled in 1997, the prevalence of deficiency, defined as <17.5 nmol/L, was 2.8%, but the prevalence of insufficiency, defined as 70 yr 15.0 µg /day
Women
19-30 yr 5.0 µg /day
31-50 yr 5.0 µg /day
51-70 yr 10.0 µg /day
>70 yr 15.0 µg /day
Rationale: The AI for younger adults (19-50 years) is based on the amount of vitamin D required to maintain serum 25(OH)D at a level of at least 27.5 nmol/L with minimal exposure to sunlight. One study of US women of this age (Kinyamu et al 1997) showed that an average intake of 3.3-3.4 µg/day resulted in serum 25(OH)D of greater than 30 nmol/L. A study of females in Australia undertaken across both the summer and winter months at latitude 38o (Pasco et al 2001), assessed median intakes to be only 1.3 µg/day (much lower than other estimates for Australia and New Zealand), but had only 7% of subjects with serum 25(OH)D below 28 nmol/L in summer and 11% in winter. A vitamin D intake of 2.5 µg/day was seen as prudent for this age group. There are no data on men on which to set a figure except from one study of submariners not exposed to sunlight, whose status was assessed with or without a 15 µg/day supplement (Holick, 1994). However, the effects of lower doses were not assessed in this study. It is therefore assumed that requirements for men will be the same as those for women.

To cover the needs of all adults in the age range of 19-50 years, regardless of exposure to sunlight and in recognition of the fact that the available data were collected in women, a figure of 5 µg/day was set as the AI for younger adults. The AI was raised to 10 µg/day for adults aged 51-70 years to account for the reduced capacity for the skin to produce vitamin D with ageing (Holick et al 1989, Need et al 1993). Data on bone loss and vitamin D supplementation in women were also taken into consideration (Dawson-Hughes et al 1991, 1995). For adults over 70 years, the AI was raised to 15 µg/day. Studies of elderly people with intakes of 9.6 µg, 7.1 µg or 5.2 µg vitamin D/day showed that 8, 14 and 45%, respectively had low levels of serum 25(OH)D (Gloth et al 1995, Kinyamu et al 1997, O’Dowd et al 1993). A value of 7.5 µg/day was considered prudent for those with limited sun exposure and was doubled to 15 µg/day to cover the needs of all adults of this age, regardless of sun exposure or body stores.

It should be noted that the effect of increasing the dietary intake of vitamin D on 25(OH)D concentration in blood varies according to the existing vitamin D status of the individual. The status of those with low 25(OH)D levels in plasma will be improved to a more significant degree than of those with pre-existing high status (eg plasma levels above about 50 nmol/L) who may benefit little from the additional dietary intake.

Role of sunlight exposure: There is evidence from selected subpopulations that about 4-8% of adults in Australia have serum 25(OH)D levels below 28 nmol/L and about 30% have levels below 50 nmol/L. (Pasco et al 2001, MacGrath et al 2001, Vasikaran et al 2000). National surveys in New Zealand have indicated that some 2.8% of adults have levels of less than 17.5 nmol/L and 27.6% have levels below 37.5 nmol/L. Both sunlight and diet play an essential role in vitamin D status in younger adults. Kimlin et al (2003) estimated that for an older woman with fair skin, exposure of 6% of the body surface (face, hands, forearm) to sunlight for 15-30 minutes, 2-3 times per week would provide the equivalent of 15 µg vitamin D/day. Because of reduced cutaneous production, young adults (19-50 years) who live in southern latitudes such as Tasmania and the southern island of New Zealand are particularly at risk of becoming vitamin D deficient during the winter months.

For dark-skinned peoples such as indigenous Australians and New Zealanders and certain migrant groups and veiled women, there is evidence in Australia of high rates of vitamin D deficiency. Grover et al (2001) found that 80% of pregnant dark-skinned, veiled women attending one antenatal clinic in a large teaching hospital had vitamin D levels of less than 22 nmol/L. For people with little access to sunlight a supplement of 10 µg/day would not be excessive.

Institutionalised elderly: Several studies in Australia and New Zealand have shown high rates of deficiency in very elderly people with restricted access to sunlight, many of whom live in institutions. Estimates of deficiency range from 15-52% in Australia (Bruce et al 1999, Flicker et al 2003, Inderjeeth et al 2000, Stein 1996). Ley et al (1999) found that 49% of older New Zealand subjects in winter and 33% in summer had low serum 25(OH)D while McAuley et al (1997) reported 69% of subjects in Dunedin having low levels in winter, but only 26% in summer. Data from the National Nutrition Survey of New Zealand (Green et al 2004b) showed that 1.6% of males over 65 years and 5.8% of females had blood levels below 17.5 nmol/L for serum 25(OH)D and that 20.5% of men and 39.6% of women had levels below 37.5 nmol/L. This survey did not include institutionalised people. The recommendation of 15 µg/day for those over 70 years relates to the general population over 70 years. A number of recent studies demonstrate protection from falls and fractures with supplemental intakes of vitamin D in the elderly.

For institutionalised or bed-bound elderly who have very restricted exposure to sunlight often accompanied by reduced food intake, supplementation with vitamin D in the order of 10-25 µg/day may be necessary (Brazier et al 1995, Byrne et al 1995, Chapuy et al 1992, Egsmose et al 1987, Fardellone et al 1995, Kamel et al 1996, McKenna 1992, Sebert et al 1995, Sorva et al 1991).

Pregnancy

Age AI
14-18 yr 5.0 µg/day
19-30 yr 5.0 µg/day
31-50 yr 5.0 µg/day
Rationale: Although there is placental transfer of vitamin D and its metabolites from mother to foetus, the amounts are too small to affect the mother’s vitamin D requirement, particularly as there is a rise in serum calcitriol (probably of placental origin) and a rise in calcium absorption in late pregnancy (Paunier et al 1978, Specker 2004). However, maternal deficiency of vitamin D can affect the foetus and needs to be prevented. Pregnant women who receive regular exposure to sunlight do not require supplementation. However, at intakes of less than 3.8 µg/day, pregnant women in winter months at high latitudes have been shown to have low serum 25(OH)D (Paunier et al 1978). For women who have little access to sunlight, a supplement of 10 µg/day prenatally would not be excessive. In the last trimester of pregnancy there is quite a large transfer of 25(OH)D across the placenta.

Lactation

Age AI
14-18 yr 5.0 µg/day
19-30 yr 5.0 µg/day
31-50 yr 5.0 µg/day
Rationale: There is no evidence that lactation increases the AI of the mother for vitamin D. Thus, if sunlight is inadequate, an AI of 5 µg/day is needed. As noted above, the infants of dark-skinned and/or veiled women may be at higher risk of developing rickets partly because of marginal or frank vitamin D deficiency in the mother. For mothers and their babies with limited exposure to sunlight, a supplemental intake during lactation of 10 µg/day would not be excessive.

Upper Level of Intake

Age UL
Infants
0-12 months 25 µg /day
Children and adolescents
1-3 yr 80 µg/day
4-8 yr 80 µg/day
9-13 yr 80 µg/day
14-18 yr 80 µg/day
Adults 19+ yr
Men 80 µg/day
Women 80 µg/day
Pregnancy
14-18 yr 80 µg/day
19-50 yr 80 µg/day
Lactation
14-18 yr 80 µg/day
19-50 yr 80 µg/day
Rationale: The UL for infants was set on the basis of a NOAEL of 45 µg/day (Fomon et al 1966, Jeans & Stearns 1938) together with a UF of 1.8 (FNB:IOM 1997) because of the small sample sizes and insensitivity of the endpoint used (linear growth). For children and adolescents, there are little available data, so the recommendation for adults was adopted.

The UL for adults was based on studies assessing the effect of vitamin D on serum calcium in humans (Honkanen et al 1990, Johnson et al 1980, Narang et al 1984, Vieth et al 2001). Johnson et al (1980) and Honkanen et al (1990) conducted studies with supplementation at 50 µg/day or 45 µg/day for several months and saw no adverse effects. Narang et al (1984), using dosages of 60 µg and 95 µg/day over several months in a non-randomised trial that included 30 normal controls, saw increases above 2.75 mmol/L in serum calcium levels a level considered as defining hypercalcaemia, at 95 µg/day but not at 60 µg/day. However, a recent, well-designed, RCT by Vieth et al (2001) saw no adverse effect of dosages of 25 µg/day or 100 µg/day over six months in 30 subjects. This finding was confirmed in a later randomised study (Vieth et al 2004) of inpatients with subclinical or marginal deficiency. Vieth et al (2001) felt that the earlier data of Narang et al (1984) may have been erroneous in dosage, citing concerns about lack of independent confirmation of the actual amount of vitamin D administered (there were no measures of serum 25(OH)D). There is also some animal evidence of oral vitamin D causing non-calcified atherosclerosis of large arteries (Taura et al 1979, Toda et al 1985), suggesting that a cautious approach should be taken to high dose vitamin D in people other than the elderly.

Taking all of this into account, the figure of 100 µg/day from Vieth’s studies was adopted as the NOAEL and a UF of 1.2 was applied because of the inconsistencies in the studies and they were performed on relatively small number of subjects with pre-existing marginal vitamin D status. Vieth et al (2001) have themselves cautioned about the relatively small numbers in their studies.

The available data for pregnancy and lactation are inadequate to derive a figure different from that of other adults. There appears to be no increased sensitivity during these physiological states.

It should be noted that the intake of vitamin D via food would add to the vitamin D formed by exposure to sunlight.

( References provided upon Request from Jerry )

DRUG WAR FACTS SPEAK VOLUMES FOR THE IDIOCY OF CURRENT DRUG POLICY

Posted in WAR ON DRUGS with tags , , , , on October 6, 2013 by drjgelb

What can you do to encourage rational drug policy development?

Read the “Drug War Facts” book or Website so that you can take on discussion or debate on drug policy with confidence. Armed with the facts means emotive, hysterical and exaggerated arguments are totally unnecessary. The facts are so compelling as to shine a bright spotlight on the ideological, harmful and moronic drug policies known collectively worldwide as the “War on Drugs”. Here’s an idea to contemplate: A criminal named Richard M Nixon declared WAR ON DRUGS in 1970, without support from the vast majority of Medical experts. He possessed a vast knowledge and understanding of American History and was very familiar with the catastrophic impact of policies of Alcohol Prohibition imposed by the U.S. Government between 1920 and 1932. In those 12 short years, the American Mafia took control of every aspect of the Alcohol industry, from brewing, to transport, distribution, wholesale and retail sales, entertainment venues and bars and ensured public access to these venues by whatever means necessary……be it bribing law enforcement to look the other way, or constructing elaborate tunnels beneath city streets to link mob owned bars and clubs without putting patrons at risk of arrest and prosecution. And with such a monopoly, how much profit did the Mafia earn during “Prohibition”?

$2 Billion in 1920’s dollars!! Worth today an estimated $350,000,000,000!

This money bought the Mafia unprecedented Police co-operation and protection as well as political influence at the highest level, for the next 75yrs and supported a criminal enterprise that became, in New York at least, a rival underground government many times more deadly than that of the worst banana republic.

So here are the latest figures regarding the U.S. State & Federal war on its citizens:

WHAT’S NEW AT DRUG WAR FACTS – VOL. 3, NO. 9, OCTOBER 2013

ISSUE IN FOCUS: DRUG ARRESTS

The FBI recently released its Uniform Crime Report for 2012. They estimate that of the total 12,196,959 criminal arrests in the US that year, 1,552,432 were for drug violations. They further report that 82.2% of those, or 1,276,099 drug arrests, were for possession. To put these numbers in context, in 2012 US law enforcement also made an estimated 521,196 arrests for all violent crimes and 1,646,212 arrests for all property crimes.

In 2013, Professor Harry Levine of CUNY-Queens College estimated that on average, a marijuana possession arrest in New York City takes about 2.5 hours of police time. New York state essentially decriminalized simple marijuana possession in 1977.

[http://www.drugwarfacts.org/cms/node/3187#sthash.jnpMxMoa.dpbs]

If each drug possession arrest in the US took only 2.5 hours of police time, then it would mean 3,190,247.5 hours of police time were wasted in 2012 arresting drug users just for the crime of using drugs – not trafficking, not manufacture, just possession.

Next, consider this set of numbers. According to the FBI’s new UCR, quote: “In the nation in 2012, 46.8 percent of violent crimes and 19.0 percent of property crimes were cleared by arrest or exceptional means.” End quote. Those clearance rates are typical, in fact that’s the best property crime clearance rate in at least a decade and a half.

[http://www.drugwarfacts.org/cms/node/3493#sthash.0n5HWbtd.dpbs]

Marijuana arrests totaled 749,825 in 2012, down slightly from 2011’s total of 757,969. Marijuana possession accounted for 658,231 arrests – again slightly down from the 2011 total of 663,032. Looking at the year-to-year changes in arrest figures doesn’t reveal much, but examining data from several years can reveal trends. For example, in 2001, the U.S. had 1,586,902 criminal drug arrests out of a total 13,699,254 arrests. Of the drug arrests. 19.4 percent were for sale or manufacture, while the remaining 80.6% were for possession. In 2012, as I noted earlier, the 1,552,432 criminal drug arrests were 17.8 percent sale or manufacture and the remaining 82.2 percent were for possession. Back in 2001, 9.7 percent of all drug arrests were for sale or manufacturing of heroin,
cocaine, or their derivatives and 40.4 percent were for simple possession of marijuana. In 2012, only 6.1 percent of all drug arrests were for sale or manufacturing of heroin, cocaine, or their derivatives, and 42.4 percent were for simple possession of marijuana.

From 2003 through 2007, the US saw a rapid escalation in drug arrests. In 2003, the number jumped to 1,678,192 from 1,538,813 in 2002, then to 1,746,570 in 2004. Drug arrests in 2005-2007 topped 1.8 million per year, peaking in 2006 at1,889,810 drug arrests. The decline started in 2008, when US law enforcement made only 1,702,537 drug arrests.

http://www.drugwarfacts.org/cms/node/235#sthash.V2SF6wK6.j2I3uzQy.dpbs

“DEFELONISATION” – NEW WORD, NEW WORLD?

Posted in WAR ON DRUGS with tags , , , on October 5, 2013 by drjgelb

Today, comes news from “stopthedrugwar.org” that adds a further increment of hope to the mounting pile slowly accumulating on politicians’ doorsteps.

http://stopthedrugwar.org/chronicle/2013/oct/02/defelonization_next_step

“Defelonization”–The Next Step in Winding Down the Drug War.

Defelonization (with an “s” in Australia!) of drug possession is starting to take hold across the country. California looks set to join the list of states easing up, and Washington state could be next. Thirteen states, the District of Columbia, and the federal government have already passed laws making simple drug possession a misdemeanor instead of a felony, and the momentum appears to be growing. A bill in California to do something similar has passed the legislature and is currently sitting on the governor’s desk, and efforts are afoot to push a defelonization measure through the Washington legislature next year.

An overcrowded California prison (supremecourtus.gov)

Such measures are designed to ease prison overcrowding, ease pressures on budgets, and help drug users by avoiding saddling them with felony convictions. They also reflect increasing frustration with decades of drug prohibition efforts that have failed to stop drug use, but have resulted in all sorts of collateral costs. In California alone, even after Gov. Jerry Brown’s (D) prison realignment scheme, more than 4,000 people remain in state prisons on simple drug possession charges. At $47,000 per inmate per year [8], that comes out to more than a $200 million annual bill to state taxpayers. Under current California law, people convicted of a drug possession felony can be sentenced to up to three years in prison. More than 10,000 people are charged with drug possession felonies each year, although many of them receive probation if convicted.

California state Sen. Mark Leno (D-San Francisco) moved to redress that situation with Senate Bill 649 [9], which passed the legislature on the final day of the session. The bill is not a defelonization bill per se; instead, it makes drug possession a “wobbler,” meaning it provides prosecutors with the flexibility to charge drug possession as either a felony or a misdemeanor. “Our system is broken,” said Lynne Lyman, California state director for the Drug Policy Alliance [10], which supported the bill. “Felony sentences don’t reduce drug use and don’t persuade users to seek treatment, but instead, impose tremendous barriers to housing, education and employment after release — three things we know help keep people out of our criminal justice system and successfully reintegrating into their families and communities.”

Even Republicans got on board with the bill, helping to get it through the Assembly earlier this year.

California state Sen. Mark Leno (wikipedia.org); “I am proud that we got bipartisan support in the Assembly,” Leno told the Chronicle. The bill currently awaits Gov. Brown’s signature, and although his signature is not required for it to become law, Leno said he believed the governor would act on it, and he urged supporters to let the governor know now that they want him to sign it. “Anyone can go to the governor’s web site [11] and offer support through an email communication,” Leno said. “I am always hopeful he will sign it.”

While Californians wait for the governor to act (or not), activists and legislators in Washington are gearing up to place a defelonization bill before the legislature there next year. Sensible Washington [12], the activist group behind the effort, says it has lined up legislative sponsors for the bill and will pre-file in December for next year’s legislative session. State Rep. Sherry Appleton (D-Poulsbo) will be the primary sponsor of this proposal in the House. Reps. Joe Fitzgibbon (D-Burien), Jim Moeller (D-Vancouver), Jessyn Farrell (D-Seattle), and Chris Reykdal (D-Tumwater) have all signed on as official cosponsors, with more to be announced soon. Sensible Washington hopes to have a companion bill filed simultaneously in the Senate.

Under current Washington law, the possession of any controlled substance (or over 40 grams of cannabis) is an automatic felony. Under this new proposal, the possession of a controlled substance — when not intended for distribution — would be reduced from a felony charge, to a misdemeanor (carrying a maximum sentence of 90 days, rather than five years). Laws regarding minors would not be affected. “Removing felony charges for simple drug possession is a smart, pragmatic approach to reducing some of the harms associated with the war on drugs,” said Anthony Martinelli, Sensible Washington’s communications director. “The goal is to stop labeling people as felons, filling up our prisons and ruining their lives in the process, for possessing a small amount of an illegal substance.”

He elaborated in a Tuesday interview with the Chronicle.

“We support full decriminalization, like the Portuguese model, but defelonization is a big step forward, and we feel that the public and lawmakers are ready for it,” he said. “We have to find a way to deal with the dangers of the war on drugs. Another reason is the massive disparity in our cannabis law — an ounce is legal, but an ounce and a half is a felony. This would remove felonies for cannabis possession, but we don’t think anyone should be hit over the head with a felony for personal drug possession.”Martinelli said Sensible Washington and its allies would be spending the next few months preparing to push the bill through the legislature. “We will be building public and legislative support, continuing to work on garnering media attention, activating our base, and getting more lawmakers on board,” he said. “We’re really trying to form a bipartisan coalition and get other organizations involved as well.”

One of those groups is the ACLU of Washington [13]. Sensible Washington and the ACLU of Washington were bitter foes in the fight over the state’s successful I-502 marijuana legalization initiative — Sensible Washington opposed it as a half-measure that endangered medical marijuana, a claim that ACLU and other advocates contested — but appear to be on the same page when it comes to this sentencing reform. “We support the decriminalization of drug use”, said Alison Holcomb, criminal justice project director for the ACLU of Washington. “We’re looking forward to working in collaboration with Sensible and its allies to achieve that goal.” Martinelli said he could now announce that the proposed bill has picked up its first Senate sponsor, Sen. Jeanne Kohl-Welles (D), to add to its growing list of House sponsors.

Missing from that list of House sponsors is one of the most prominent drug reformers in the House, Rep. Roger Goodman (D-Kirkland), the chairman of the House Public Safety Committee, but that’s not because he opposes the idea, Goodman told the Chronicle Tuesday. “As chair of the committee, it’s important for me to be an honest broker to get legislation through,” Goodman explained. “My position as chair is weakened if there is a potentially controversial issue and I’m seen as being on one side of it. It’s not that I oppose it, and I certainly will hold a hearing on it and move it, but my role is more to facilitate negotiations on provisions of the bill without being an interested party,” he said. “It is an idea that is certainly worth pursuing”, he said. “We need to reprioritize. The tough penalties we impose on people for merely possessing drugs is so arbitrary compared to the penalties for other offenses where there is direct physical harm perpetrated against others,” Goodman said. “And by now, we all acknowledge that drug possession is not merely an indiscretion, but might be linked to behavioral health issues. Our approach should be to facilitate therapeutic interventions. We have deferred prosecution programs already, but only for alcohol. Those arrested for drug possession are not eligible because it’s a felony. If we could make deferred prosecution available for drug cases, we could make much more headway on the problem,” he said. “And doing so would only codify what is already often existing practices”,he said. “Many or most courts and prosecutors are already pleading down felony drug cases to misdemeanors because of budget constraints and space limitations in the jails,” Goodman noted. “We can change the law to conform with that practice without an additional threat to public safety. Beyond that, we could remove the prejudicial effect of a felony conviction when it is so evident they hinder people from reintegrating into the community.”

While Sensible Washington and its allies are moving full steam ahead, passing the bill could be a multi-year effort, Goodman warned. “I anticipate prosecutors saying that if we set a certain possession threshold, drug dealers will make sure they possess no more than that amount and will play the system,” he said. “We have to figure out a way to find a threshold or divide possession cases into degrees. I hear the concern, but I’m not sure what the solution is. But this is a next important phase of drug policy reform: cranking down the drug war yet one more notch and doing what’s rational and fiscally responsible.” “There is lots of work to be done. We’ll see how this plays out in the legislature. It’s probably going to need more lobbying and more background discussion among more legislators,” he predicted. “So far, it’s not a real prominent topic, so it might end up being a work in progress. But who knows? It might catch on fire, and we’ll get a quick consensus.”

Defelonization News Feature State & Local Executive Branches State & Local Legislatures Washington Initiative 502
StoptheDrugWar.org • P.O. Box 18402 • Washington DC 20036
Phone (202) 293-8340 • Fax (202) 293-8344 • Email • Privacy Policy
Source URL: http://stopthedrugwar.org/chronicle/2013/oct/02/defelonization_next_step
Links:
[1] http://stopthedrugwar.org/user/psmith
[2] http://stopthedrugwar.org/chronicle/803
[3] http://stopthedrugwar.org/taxonomy/term/255
[4] http://stopthedrugwar.org/taxonomy/term/92
[5] http://stopthedrugwar.org/taxonomy/term/156
[6] http://stopthedrugwar.org/taxonomy/term/45
[7] http://stopthedrugwar.org/taxonomy/term/246
[8] http://www.lao.ca.gov/laoapp/laomenus/sections/crim_justice/6_cj_inmatecost.aspx
[9] http://www.leginfo.ca.gov/pub/13-14/bill/sen/sb_0601-0650/sb_649_bill_20130912_enrolled.pdf

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