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Calcium

The Calcium fraud and what you need to know!

Saul Yudelowitz Bsc (Hons)

I have been working with professional athletes and the general public for 10 years now. In this time I have seen and learnt quite a lot but I have always been surprised as to what some of the advice to the public, regarding their health.
 
 Below is a collection of the effects of calcium supplementation. Do remember that we need calcium, the question is how much and do you really need to take calcium supplements and vitamin D?
 
You should use the information below to make informed choices about any changes to your health regime. Question everything including what we say, don’t every just accept what is told to you at face value.
 
 

In Breast Cancer a Calcium Pump Works both Ways

By HospiMedica International staff writers Posted on 08 Nov 2010

Cancer researchers have identified a protein overexpressed in breast cancer cells that functions both as a calcium pump and as a component of a signaling system, which triggers a massive cellular influx of calcium.

The protein, Secretory Pathway Ca2+-ATPase (SPCA2), was thought to be a supplemental protein pump – one of several able to force calcium ions out of the cell. However, a study published in the October 1, 2010, issue of the journal Cell revealed that SPCA2 primarily acted in an opposite fashion.

Investigators at Johns Hopkins University (Baltimore, MD, USA) showed that in breast cancer cells SPCA2 moved from its normal location in the cytoplasm to the cell surface, where it interacted with calcium channels. SPCA2 activated the channels, admitting large quantities of calcium into the cells.

The action of SPCA2 in breast cancer cells was thought to have derived from a possible role in lactation, a function of normal breast tissue. “Human milk is extremely high in calcium, and all that calcium gets there because SPCA2, along with an elaborate network of other proteins, is turned on during lactation,” explained senior author Dr. Rajini Rao, professor of physiology at Johns Hopkins University. “SPCA2’s normal purpose, we think, is to signal calcium channels to open so lots and lots of calcium come into the cells of mammary tissue, where it is packaged and pumped out to the milk.”

The SPCA2 gene is down regulated in normal breast tissue except during lactation. However, it is highly up regulated in breast cancer cells. “When regulation of SPCA2 goes wrong, that is when you have breast cancer,” said Dr. Rao, “probably because in breast tumor cells, the lack of regulation of the pump/signaling mechanism lets vast amounts of calcium into the cells, which stimulates the cell cycle, and triggers high levels of proliferation.”

Related Links:

JohnsHopkins University

 

Nutr Res. 2008 May;28(5):285-92.

 
 
 

Calcium and vitamin D intakes may be positively associated with brain lesions in depressed and nondepressed elders.

Payne ME, Anderson JJ, Steffens DC.

Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA. martha.payne@duke.edu

Comment in:

Nutr Res. 2008 Nov;28(11):809; author reply 809-10.

Abstract

Studies indicate that diet and vascular calcification may be related to the occurrence of brain lesions, although the importance of dietary calcium and vitamin D has not been investigated. The objective of this study was to test the hypothesis that calcium and vitamin D intakes would be positively associated with brain lesion volumes in elderly individuals with and without late-life depression. A cross-sectional study was performed as part of a longitudinal clinical study of late-life depression. Calcium and vitamin D intakes were assessed in 232 elderly subjects (95 with current or prior depression, 137 without depression) using a Block 1998 food frequency questionnaire. Calcium, vitamin D, and kilojoule intake were determined. Brain lesion volumes were calculated from magnetic resonance imaging scan. Subjects were 60 years or older. Calcium and vitamin D intakes were significantly and positively correlated with brain lesion volume (P < .05 and P < .001, respectively). In 2 separate multivariable models, controlling for age, hypertension, diabetes, heart disease, group (depression/comparison), lesion load (high/low), and total kilocalories, these positive associations remained significant (P < .05 for calcium; P < .001 for vitamin D). In conclusion, calcium and vitamin D consumption were associated with brain lesions in elderly subjects even after controlling for potentially explanatory variables. These associations may be due to vascular calcification or other mechanism. The possibility of adverse effects of high intakes of calcium and vitamin D needs to be further explored in longitudinal studies of elderly subjects.

PMID: 19083421 [PubMed - indexed for MEDLINE]PMCID: PMC2516961
 
 
 
 

Dairy, calcium, and vitamin D intakes and prostate cancer risk in the National Health and Nutrition Examination Epidemiologic Follow-up Study cohort1,2,3

Marilyn Tseng, Rosalind A Breslow, Barry I Graubard and Regina G Ziegler

1 From the Division of Population Science, Fox Chase Cancer Center, Philadelphia, PA (MT); the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD (RAB); and the Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (BIG and RGZ)

Background: Dairy intake may increase prostate cancer risk, but whether this is due to calcium's suppression of circulating vitamin D remains unclear. Findings on calcium and vitamin D intake and prostate cancer are inconsistent.

Objective: We examined the association of dairy, calcium, and vitamin D intake with prostate cancer.

Design: In a prospective study of 3612 men followed from 1982–1984 to 1992 for the first National Health and Nutrition Examination Epidemiologic Follow-up Study, 131 prostate cancer cases were identified. Dietary intake was estimated from questionnaires completed in 1982–1984. Relative risk (RR) and 95% CIs were estimated by using Cox proportional hazards models adjusted for age, race, and other covariates.

Results: Compared with men in the lowest tertile for dairy food intake, men in the highest tertile had a relative risk (RR) of 2.2 (95% CI: 1.2, 3.9; trend P = 0.05). Low-fat milk was associated with increased risk (RR = 1.5; 95% CI: 1.1, 2.2; third compared with first tertile; trend P = 0.02), but whole milk was not (RR = 0.8; 95% CI: 0.5, 1.3; third compared with first tertile; trend P = 0.35). Dietary calcium was also strongly associated with increased risk (RR = 2.2; 95% CI: 1.4, 3.5; third compared with first tertile; trend P = 0.001). After adjustment for calcium intake, neither vitamin D nor phosphorus was clearly associated with risk.

Conclusions: Dairy consumption may increase prostate cancer risk through a calcium-related pathway. Calcium and low-fat milk have been promoted to reduce risk of osteoporosis and colon cancer. Therefore, the mechanisms by which dairy and calcium might increase prostate cancer risk should be clarified and confirmed.

Key Words: Dairy • diet • calcium • vitamin D • prostatic neoplasms

JAMA. 2006 Apr 19;295(15):1793-800.
 
 
 

Education, 15-year risk factor progression, and coronary artery calcium in young adulthood and early middle age: the Coronary Artery Risk Development in Young Adults study.

Yan LL, Liu K, Daviglus ML, Colangelo LA, Kiefe CI, Sidney S, Matthews KA, Greenland P. Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Ill 60611, USA. lijing@northwestern.edu

Abstract

CONTEXT: The inverse association between education and cardiovascular disease is well established, but little is known about the relationship between education and subclinical disease, which is free from medical access and treatment-related influences, or about possible mediating pathways for these relationships.

OBJECTIVE: To examine the association of education with coronary artery calcium (CAC), an indicator of subclinical atherosclerosis, and cardiovascular risk factors, and their changes as potential mediators.

DESIGN, SETTING, AND PARTICIPANTS: A population-based, prospective, observational study (Coronary Artery Risk Development in Young Adults [CARDIA]) of 2913 eligible participants (44.9% black; 53.9% women) recruited from 4 metropolitan areas (Birmingham, Ala; Chicago, Ill; Minneapolis, Minn; and Oakland, Calif) in both the baseline (1985-1986, ages 18-30 years) and year 15 examinations (2000-2001, ages 33-45 years). Education (year 15) was classified into less than high school (n = 128), high school graduate (n = 498), some college (n = 902), college graduate (n = 764), and more than college (n = 621).

MAIN OUTCOME MEASURE: Presence of CAC, measured twice by computed tomography (mean total Agatston score >0) at year 15.

RESULTS: Overall CAC prevalence in this sample was 9.3%. After adjusting for age, race, and sex, the odds ratios (ORs) for having CAC were 4.14 (95% confidence interval [CI], 2.33-7.35) for less than high school education, 1.89 (95% CI, 1.23-2.91) for high school graduate, 1.47 (95% CI, 0.99-2.19) for some college, and 1.24 (95% CI, 0.84-1.85) for college graduate compared with those participants with more than a college education (P for trend<.001). This was also consistent within each of the 4 race-sex groups. Adjustment for baseline systolic blood pressure, smoking, waist circumference, physical activity, and total cholesterol reduced the ORs to 2.61 (95% CI, 1.40-4.85) for less than high school, 1.38 (95% CI, 0.88-2.17) for high school graduate, 1.17 (95% CI, 0.78-1.77) for some college, and 1.13 (95% CI, 0.76-1.69) for college graduate compared with more than a college education (P for trend = .01), and only slightly attenuated by further adjustment for 15-year changes in risk factors.

CONCLUSION: Education was inversely associated with the prevalence of CAC, an association partially explained by baseline risk factors and minimally by 15-year changes in risk factors.

PMID: 16622141 [PubMed - indexed for MEDLINE]Free Article
 
 
 
 

Calcium and vitamin D intakes may be positively associated with brain lesions in depressed and nondepressed elders.

Payne ME, Anderson JJ, Steffens DC.

Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC 27710, USA. martha.payne@duke.edu

Comment in:

Nutr Res. 2008 Nov;28(11):809; author reply 809-10.

Abstract

Studies indicate that diet and vascular calcification may be related to the occurrence of brain lesions, although the importance of dietary calcium and vitamin D has not been investigated. The objective of this study was to test the hypothesis that calcium and vitamin D intakes would be positively associated with brain lesion volumes in elderly individuals with and without late-life depression. A cross-sectional study was performed as part of a longitudinal clinical study of late-life depression. Calcium and vitamin D intakes were assessed in 232 elderly subjects (95 with current or prior depression, 137 without depression) using a Block 1998 food frequency questionnaire. Calcium, vitamin D, and kilojoule intake were determined. Brain lesion volumes were calculated from magnetic resonance imaging scan. Subjects were 60 years or older. Calcium and vitamin D intakes were significantly and positively correlated with brain lesion volume (P < .05 and P < .001, respectively). In 2 separate multivariable models, controlling for age, hypertension, diabetes, heart disease, group (depression/comparison), lesion load (high/low), and total kilocalories, these positive associations remained significant (P < .05 for calcium; P < .001 for vitamin D). In conclusion, calcium and vitamin D consumption were associated with brain lesions in elderly subjects even after controlling for potentially explanatory variables. These associations may be due to vascular calcification or other mechanism. The possibility of adverse effects of high intakes of calcium and vitamin D needs to be further explored in longitudinal studies of elderly subjects.

PMID: 19083421 [PubMed - indexed for MEDLINE]PMCID: PMC2516961

 
 
 
Calcium in Ischemic Cell Death

Tibor Kristián, PhD; Bo K. Siesjö, MD, PhD

From the Center for the Study of Neurological Disease, The Queen's Medical Center, Honolulu, Hawaii.

Correspondence to Tibor Kristián, PhD, Center for the Study of Neurological Disease, The Queen's Medical Center, University Tower 8th Floor, 1356 Lusitana St, Honolulu, HI 96813. E-mail tibor@www.cns.queens.org

Background—This review article deals with the role of calcium in ischemic cell death. A calcium-related mechanism was proposed more than two decades ago to explain cell necrosis incurred in cardiac ischemia and muscular dystrophy. In fact, an excitotoxic hypothesis was advanced to explain the acetylcholine-related death of muscle end plates. A similar hypothesis was proposed to explain selective neuronal damage in the brain in ischemia, hypoglycemic coma, and status epilepticus.

Summary of Review—The original concepts encompass the hypothesis that cell damage in ischemia-reperfusion is due to enhanced activity of phospholipases and proteases, leading to release of free fatty acids and their breakdown products and to degradation of cytoskeletal proteins. It is equally clear that a coupling exists between influx of calcium into cells and their production of reactive oxygen species, such as ·O2-, H2O2, and ·OH. Recent results have underscored the role of calcium in ischemic cell death. A coupling has been demonstrated among glutamate release, calcium influx, and enhanced production of reactive metabolites such as ·O2-, ·OH, and nitric oxide. It has become equally clear that the combination of ·O2- and nitric oxide can yield peroxynitrate, a metabolite with potentially devastating effects. The mitochondria have again come into the focus of interest. This is because certain conditions, notably mitochondrial calcium accumulation and oxidative stress, can trigger the assembly (opening) of a high-conductance pore in the inner mitochondrial membrane. The mitochondrial permeability transition (MPT) pore leads to a collapse of the electrochemical potential for H+, thereby arresting ATP production and triggering production of reactive oxygen species. The occurrence of an MPT in vivo is suggested by the dramatic anti-ischemic effect of cyclosporin A, a virtually specific blocker of the MPT in vitro in transient forebrain ischemia. However, cyclosporin A has limited effect on the cell damage incurred as a result of 2 hours of focal cerebral ischemia, suggesting that factors other than MPT play a role. It is discussed whether this could reflect the operation of phospholipase A2 activity and degradation of the lipid skeleton of the inner mitochondrial membrane.

Conclusions—Calcium is one of the triggers involved in ischemic cell death, whatever the mechanism.

Key Words: calcium • cerebral ischemia • free radicals • mitochondria
 
 

Calcium pills 'increase' risk of heart attack

By Emma Wilkinson Health reporter, BBC News

Calcium supplements are commonly taken by older people at risk of fracture

Calcium supplements taken by many older people could be increasing their risk of a heart attack, research shows.

The study, in the British Medical Journal, said people who took supplements were 30% more likely to have a heart attack.

Data from 11 trials also suggested the medicines were not very effective at preventing bone fractures.

Almost 3m people in the UK are thought to have osteoporosis and many take calcium pills to prevent fractures.

The study recommends doctors review their use of calcium supplements for managing osteoporosis.

The National Osteoporosis Society said most people should be able to get enough calcium through their diets, rather than reaching for the medicine cabinet.

The researchers said those who had a diet naturally high in calcium were at no increased danger.

'Limited benefit'

In all 12,000 people aged over 40 took part in the trials of calcium supplements of 500mg or more a day.

It is a balance of risks - people should consider the risks involved and how they apply to their own circumstances and discuss the matter with their GP” says Dr Alison Avenell Study author

The risk of heart attack was seen across men and women, was independent of age and the type of supplement given.

A small increased risk of death was seen in the study but was not statistically significant, the researchers said.

The reason for the increased risk of heart attack is not clear but it is thought the extra calcium circulating in the blood could lead to a hardening of the arteries.

Calcium in the diet is safe and the Food Standards Agency recommends adults have 700mg of calcium a day from milk, cheese and green, leafy vegetables.

Dr Alison Avenell, from the University of Aberdeen which did the research with colleagues in New Zealand and the US, said the evidence suggests calcium supplements only have a limited benefit in preventing fractures, especially when compared to other treatments available.

"It is a balance of risks - people should consider the risks involved and how they apply to their own circumstances and discuss the matter with their GP," she said.

She added the results did not necessarily apply to younger people with conditions for which they take calcium.

Judy O'Sullivan, senior cardiac nurse at the British Heart Foundation, said the results should be interpreted with caution because the trials did not set out to look at the risk of heart attack.

"However, the research should not be completely ignored," she said.

"Any new guidelines on the prevention of fractures in those most vulnerable to them should take this type of analysis into account."

Dr Claire Bowring, of the National Osteoporosis Society, said: "We've always recommended that people should aim to get the calcium they need from their diet to help build stronger bones.

"If you get all of the calcium that you need from your diet and adequate vitamin D from exposure to sunshine, then a supplement will not be necessary."

She said there were still questions to be answered about the treatment of osteoporosis but advised people taking calcium supplements to talk to their GP, especially if they have a heart condition.

The reason for the increased risk of heart attack is not clear but it is thought the extra calcium circulating in the blood could lead to a hardening of the arteries.

Calcium in the diet is safe and the Food Standards Agency recommends adults have 700mg of calcium a day from milk, cheese and green, leafy vegetables.

Dr Alison Avenell, from the University of Aberdeen which did the research with colleagues in New Zealand and the US, said the evidence suggests calcium supplements only have a limited benefit in preventing fractures, especially when compared to other treatments available.

"It is a balance of risks - people should consider the risks involved and how they apply to their own circumstances and discuss the matter with their GP," she said.

She added the results did not necessarily apply to younger people with conditions for which they take calcium.

Judy O'Sullivan, senior cardiac nurse at the British Heart Foundation, said the results should be interpreted with caution because the trials did not set out to look at the risk of heart attack.

"However, the research should not be completely ignored," she said.

"Any new guidelines on the prevention of fractures in those most vulnerable to them should take this type of analysis into account."

Dr Claire Bowring, of the National Osteoporosis Society, said: "We've always recommended that people should aim to get the calcium they need from their diet to help build stronger bones.

"If you get all of the calcium that you need from your diet and adequate vitamin D from exposure to sunshine, then a supplement will not be necessary."

She said there were still questions to be answered about the treatment of osteoporosis but advised people taking calcium supplements to talk to their GP, especially if they have a heart condition.

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