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The “curse of morning sickness” runs in the family, according to the Daily Mail. The newspaper said that “women whose mothers suffered severe morning sickness in pregnancy are three times more likely to go through the same ordeal.”

The research behind this story analysed data from Norway’s national birth registry, investigating whether the risk of having severe morning sickness (medically known as hyperemesis gravidarum) was passed from mother to daughter. Scientists found that women had an increased risk of the problem if their mother had experienced severe morning sickness during any of her pregnancies. A history of morning sickness in the male parent’s mother made no difference to his female partner’s chances of having it, suggesting that the genetics of the foetus do not contribute to the risk. Ultimately, this study may lead to further research that can clarify whether a genetic or common environmental link explains the pattern seen.

Although milder feelings of nausea and vomiting occur in half of all pregnancies, women should consult their GP or midwife if their sickness is more severe. Medical staff can then ensure that expectant mothers maintain appropriate levels of nutrition during their pregnancy.

 

Where did the story come from?

Dr Ase Vikanes and colleagues from the Norwegian Institute of Public Health carried out this research. The study was funded by The Norwegian Research Council and published in the peer-reviewed British Medical Journal.

The research was generally covered accurately by the newspapers. However, the Daily Mail placed undue emphasis on this type of morning sickness being the result of environmental factors. This study did not provide sufficient evidence to say whether the risk of severe morning sickness is genetically passed from mother to daughter or due to a shared environmental factor.

 

What kind of research was this?

At least half of all pregnant women experience some degree of nausea and vomiting. The medical name for morning sickness, hyperemesis gravidarum, is applied to a more severe type of morning sickness which occurs in less than 2% of pregnancies. This severe morning sickness, which was the subject of this study, can lead to vitamin and nutritional abnormalities, maternal weight loss and pregnancy complications if it is not treated adequately.

This cohort study looked at whether women whose mothers had experienced this type of severe morning sickness were more likely to experience similar morning sickness during their own pregnancy.

The study also looked at whether a mother’s risk of severe morning sickness was linked to her partner’s mother having the condition during pregnancy. A theoretical cause for such a link might be that the genetic make-up of the foetus (part of which would come from its father) would influence the pregnant mother’s chance of having morning sickness.

 

What did the research involve?

The researchers used the Norwegian medical birth registry, which has kept details of all births since 1967, to study the occurrence of birth outcomes across generations. An antenatal card is completed for all pregnant women at their first routine examination during the first trimester (first 12 weeks) of pregnancy. A midwife or doctor also completes a standardised form containing demographic data on the parents, maternal health before and during pregnancy, complications and interventions during delivery and the condition of the newborn baby. In Norway, each individual also has a unique national identification number.

The study had access to data on the 2.3 million births that occurred from 1967 to 2006. Using the national identification numbers, the study linked mothers to their childbearing daughters or child-producing sons. Hyperemesis was recorded in the birth registry and classified by international disease classification codes and criteria.

They assessed three models:

• Model 1 (mother-daughter recurrence) was a woman’s risk of hyperemesis if she herself was born after a pregnancy complicated by hyperemesis.
• Model 2 (mother-son recurrence) was the risk of hyperemesis in female partners of sons who were born after a pregnancy complicated by hyperemesis.
• Model 3 (mother-daughters recurrence) was the risk of hyperemesis in a woman born after a pregnancy not complicated by hyperemesis, but whose mother had hyperemesis in a previous or subsequent pregnancy.

 

What were the basic results?

The researchers found that if a mother had hyperemesis, the risk of hyperemesis in the daughter born to that pregnancy was 3%. The risk of a daughter having hyperemesis was 1.05% if her mother did not have hyperemesis. After adjusting for potential confounding factors of maternal age at birth, time period of birth in both generations and the number of previous children the mother had given birth to, they found that the risk of hyperemesis was 2.91 times greater for daughters whose mothers had experienced hyperemesis while carrying them (odds ratio [OR] 2.91, 95% confidence interval [CI] 2.36 to 3.59).

A woman’s risk of having hyperemesis was not greater if her partner’s mother experienced hyperemesis while pregnant with him.

The researchers found that women also had an increased risk of hyperemesis if their mother had not had hyperemesis while carrying them but did have this severe morning sickness while carrying an older or younger sibling. The odds ratio for the daughter having hyperemesis if her mother had hyperemesis while carrying an older sibling was 3.18 (95% CI 1.56 to 6.49) and with a younger sibling 3.81 (95% CI 1.55 to 9.36).

 

How did the researchers interpret the results?

The researchers concluded that, “the risk of hyperemesis in a pregnant woman is threefold if the woman’s mother had ever experienced hyperemesis in a pregnancy. This was regardless of whether hyperemesis had occurred in the pregnancy leading to the woman under study or in a previous or subsequent pregnancy. In contrast, female partners of men whose mother had hyperemesis during pregnancy did not have an increased risk of hyperemesis”.

 

Conclusion

This study demonstrated a small increase in the risk of severe morning sickness (enough to cause weight loss and nutritional deficiencies) in the daughters of women who had severe morning sickness. One of this study’s strengths was that it included data from a whole population. Therefore, it did not feature any bias that may have arisen through selectively choosing only certain groups for inclusion.

However, the researchers highlight that their study did not have information on variables such as body mass index, smoking and ethnic background, which may have affected the outcomes. The Norwegian population may also have a different lifestyle and mix of ethnicities than the British population. Therefore, this study may not be directly applicable to British women.

As the researchers suggest, an increased risk across generations suggests that genetic factors may be important as the risk appears to be passed on to daughters. However, as the risk is not passed on to the female partners of sons, it is more likely that a pregnant mother’s genes have a greater effect on hyperemesis than the genetic makeup of their developing foetus. Importantly, as the researchers have also said, it is possible that the risk “is not genetically transmitted but is caused by common environmental factors that are shared by mothers and daughters”. These might be nutritional factors, other lifestyle factors or infections.

As this study did show that an increased risk was passed down from mother to daughter, further research is warranted into whether a woman’s genetic background can affect her likelihood of experiencing hyperemesis and the biological mechanisms underlying this condition.

Links To The Headlines

Mother-daughter pregnancy sickness link found. BBC News, April 30 2010

Mother’s sickly legacy: Curse of morning sickness ‘runs in the family’. Daily Mail, April 30 2010

Links To Science

Vikanes Å, Skjærven R, Grjibovski AM, et al. Recurrence of hyperemesis gravidarum across generations: population based cohort study. BMJ 2010; 340: c1640

“Babies born in the summer months have a higher risk of developing multiple sclerosis (MS) because their mothers do not get enough sun during pregnancy,” The Times reported.

This study in Australia investigated whether there is a link between the risk of developing MS and the month that people are born in. The researchers looked associations between people having MS and the levels of sunlight their mothers were likely to have been exposed to in each trimester of pregnancy.

The researchers found an association between lower ambient UV levels in the first trimester (first 12 weeks) of pregnancy and an increased risk of MS, indicating that women with babies that had been conceived in the autumn/winter months were more at risk.

There is an increasingly popular theory that MS is linked to sunlight exposure and levels of vitamin D, which is produced by the body in response to UV light. These findings appear to further support this idea. However, it is important to point out that vitamin D levels were not measured and vitamin D can be affected by several factors, including diet, lifestyle and skin type. Further research is needed in this area.

 

Where did the story come from?

The research was carried out by Dr Judith Stables and colleagues from Australian National University and the Royal Children’s Hospital, Melbourne. The study was funded by the Australian National University. The work was published in the peer-reviewed British Medical Journal.

What kind of research was this?

This retrospective cohort study investigated whether the month in which a person was born in Australia affected their risk of later developing multiple sclerosis (MS). MS becomes increasingly more prevalent the further from the equator a region lies. This has led to the theory that MS is linked to sunlight exposure and levels of vitamin D, which is produced by the body in response to UV light.

The researchers suggest that pregnant women are at particular risk of vitamin D deficiency, due to the physiological changes of pregnancy, and that they spend less time outdoors. They say that this may affect the baby’s brain development, though there is no direct evidence to support this. The researchers looked at the month of birth and risk of multiple sclerosis in Australia, a country with a large seasonal and regional variation in ambient UV levels.

It is important to consider that this type of study can only find associations between factors such as UV and disease. It cannot establish whether lack of sun exposure directly triggers the disease.

 

What did the research involve?

The researchers used data collected from a 1981 survey of MS prevalence in five Australian states. They identified the month of birth for all people with MS born between 1920 and 1950. They also identified their gender and the state in Australia in which they were born. All people with MS were interviewed and their condition verified through a medical exam, except in New South Wales where only 57% were interviewed owing to the large number of patients in this state.

A total of 1,524 people were born with MS in the five surveyed states between 1920 and 1950. As there was a small number of people with MS in each month, the researchers pooled the data into two-month groups. May-June was used as a reference period as this was the Australian winter when the ambient UV was at its lowest levels.

As a control reference group, the researchers used information from the 1981 census, including the month and location of birth for about 2.5 million people.

To estimate individuals’ exposure to UV, the researchers used the monthly averages of daily total ambient UV radiation in the capital city of each state, collected between 1996 and 2000.

 

What were the basic results?

The researchers found that the average total daily ambient UV radiation ranged from 1.6 erythemal dose units per day in Hobart, Tasmania, in July to 30.4 units per day in Perth, Western Australia, in January. An erythemal dose unit is a measure of the minimum amount of ultraviolet radiation exposure needed to induce erythema (skin redness) or sunburn.

As in previous studies, the incidence of MS was higher in women than men. Compared to that in New South Wales, the risk was lower for those born in Queensland in Northern Australia (risk ratio [RR] 0.59, 95% confidence interval [CI] 0.51 to 0.61) but higher for those born in Tasmania in Southern Australia ([RR] 2.70, 95% CI 2.06 to 3.51).

The risk of having MS was 1.23 to 1.34 times higher in people born in periods other than May-June. The highest risk was for people who had been born in the early summer months of November-December ([RR] 1.34, 95% CI 1.10 to 1.63). This pattern persisted after gender, age and region of birth were taken into account. When the risk ratio of May-June births was compared to November-December births for the different latitude regions, there was no difference in relative risk.

An analysis of stage of pregnancy and UV exposure showed there was an association between lower UV exposure and increased risk of MS in the first trimester ([RR] 0.72, 95% CI 0.62 to 0.84). However, there was no association between the UV exposure levels and risk of MS in the later months of pregnancy.

 

How did the researchers interpret the results?

The researchers said that there is an “inverse association between low ultraviolet radiation in
the first trimester and increased risk of multiple sclerosis in the offspring”. They also said that the “higher risk of multiple sclerosis for people born in November-December is consistent with these infants having experienced lower levels of ultraviolet radiation during the first trimester”.

The researchers say that as vitamin D receptors are found in cells that develop into the brain during early development of embryos, this suggests that vitamin D may play a role in brain development.

 

Conclusion

These findings suggest there is a small increase in the risk of MS for babies born in the Australian early summer with a 34% increased risk relative to the risk in people who were born in May to June (Australian winter). This corresponds to the mothers having lower exposure to ambient UV radiation levels during the first trimester of their pregnancy.

The idea that MS is linked to inadequate exposure to sunlight is growing in popularity, and these findings appear to further support this theory. The study has several limitations that should be considered when interpreting the findings:

• The researchers could not directly measure the vitamin D status of the mothers during pregnancy. Vitamin D levels are affected by exposure to UV, but also by vitamin D dietary intake, personal behaviour (such as how much time is spent outside) and the mother’s skin pigmentation. Additionally, the relationship between the mother and foetus’s vitamin D levels has not been determined in this study.
• This study was relatively small and the number of individuals that were born in each bi-monthly period was not stated. There is, therefore, a greater risk that these associations are due to chance.
• The values for the ambient UV levels were taken from averages of a period between 1996 and 2000, whereas the people with MS were born between 1920 and 1950. It is possible that UV exposure for mothers in their first trimester was different between these periods.

This study showed an association between low UV exposure in the first trimester and a small increased risk of MS. Further research would be needed to assess whether this is due to vitamin D levels and whether a mother’s exposure to the sun has any effect on her baby’s brain development that would result in increased susceptibility to MS. The causes of MS are not firmly established, but possibly involve a different susceptibility of individuals owing to their genetic makeup and exposure to environmental factors, such as viruses and vitamin D.

Vitamin D is made in the body from exposure to sunlight, but the hazards of excess exposure to UV light are well known. All people, including pregnant women, should take due precaution if spending time in the sun and should always avoid sunburn.

NICE recommend:
‘There is a need for research into the effectiveness of routine vitamin D supplementation for pregnant and breastfeeding women. Although there is some evidence of benefit from vitamin D supplementation for pregnant women at risk of vitamin D deficiency, there is less evidence in the case of pregnant women currently regarded as being at low risk of deficiency. It is possible that there will be health gains resulting from vitamin D supplementation, but further evidence is required.’

As such, pregnant women may want to take a supplement of 10 micrograms of vitamin D every day.

Women at greatest risk are advised to take this daily supplement. These include:

• women of South Asian, African, Caribbean or Middle Eastern family origin
• women who have limited exposure to sunlight, such as women who are predominantly housebound, or usually remain covered when outdoors
• women who eat a diet particularly low in vitamin D, such as women who consume no oily fish, eggs, meat, vitamin D-fortified margarine or breakfast cereal
• women with a pre-pregnancy body mass index above 30 kg/m2.’

Links To The Headlines

May birth ‘is ms risk’. Daily Mirror, April 30 2010

Babies born in summer ‘more likely to develop multiple sclerosis’. The Times, April 30 2010

Links To Science

Staples J, Ponsonby A-L, Lim L. Lowmaternal exposure to ultraviolet radiation in pregnancy, month of birth, and risk of multiple sclerosis in offspring: longitudinal analysis. BMJ 2010; 340: c1640 

A brain “pacemaker” can fight Parkinson’s disease, according to The Independent. The newspaper said that combining deep brain stimulation (DBS) implant surgery with standard drug treatment has been found to give greater improvement in motor function and to reduce symptoms more than drug treatment alone.

The research behind this news was a trial involving 366 people with advanced Parkinson’s disease that was not being adequately controlled with medication. It found that after a year, those who had a DBS implant had greater improvements in quality of life than those receiving medical treatment alone. This was particularly due to improvements in mobility, bodily discomfort and the ability to carry out the activities of daily living. However, DBS surgery was not without risks, and about 19% of patients had serious adverse effects, mainly infections.

This trial suggests that combining DBS with medication has some benefits beyond drug therapy alone. Importantly, though, DBS treatment is invasive and will not be appropriate for everyone with Parkinson’s. This means that the potential benefits of DBS would need to be balanced against its risks for each patient.

 

Where did the story come from?

This research was carried out by Professor Adrian Williams and colleagues from the Queen Elizabeth Hospital in Birmingham and other hospitals and research centres in the UK. The study was funded by the UK Medical Research Council, Parkinson’s UK and the Department of Health. It was published in the peer-reviewed medical journal, The Lancet.

The BBC News website, Daily Mail and The Independent covered this story in an accurate and balanced way. The Daily Mail and BBC News reported that this was a decade-long trial, although the trial recruited participants between 2000 and 2006, so a number of the patients will not yet have been followed for a full ten years. The current results are also only based on follow-up in the year after surgery, with longer-term results awaited. The Independent reported that 5% of people receiving DBS had severe complications, such as infections. However, 19% were reported to have serious surgery-related adverse events in the research paper.

 

What kind of research was this?

This was a randomised controlled trial (RCT) called PD-SURG, which looked at the effect of deep brain stimulation (DBS) on quality of life in people with advanced Parkinson’s disease. Treatment with DBS involves implanting wire electrodes into the brain. These electrodes are attached to a “pacemaker” device, which regularly sends electrical impulses through the electrodes and into the brain. In most cases, the pacemakers in this trial were implanted into an area of the brain known as the subthalamic nucleus, although other DBS procedures may use alternative sites.

An RCT is the most appropriate way to compare the effects of different treatments. This RCT compared the best medical treatment alone with the same type of medical treatment combined with a DBS implant. This study design would be the best way to tell whether DBS provided any additional benefits over and above standard treatment.

 

What did the research involve?

The researchers recruited 366 people with Parkinson’s disease that was not adequately controlled with medication alone. They were randomised to continue to receive best medical treatment alone (drugs such as dopamine agonists, MAO type B inhibitors, COMT inhibitors and apomorphine) or to receive DBS surgery in addition to the best medical treatment. The researchers followed the participants up for one year and measured their quality of life to see whether DBS had any effect on this outcome.

The participants in this trial were enrolled at 13 neurosurgery centres in the UK between 2000 and 2006. They had to have Parkinson’s disease diagnosed according to standard criteria, and to be fit enough to undergo surgery. Before being randomised, the participants filled out a standard Parkinson’s disease questionnaire (PDQ-39), which assessed their quality of life. One year after being randomised and receiving their assigned treatment, the participants filled in this questionnaire again.

The researchers then compared changes in quality of life in the group that received DBS and the group that did not. A change of 10 points on the questionnaire score (based on a 39-point scale) was considered to be large enough to be meaningful to patients. A secondary outcome assessed by researchers was clinical assessment of the participants’ functioning using UPDRS scores, a standard scale for measuring Parkinson’s symptoms.

As one group had surgery and the other did not, it was not possible to blind participants to which treatment they received. The researchers also knew what treatments the participants had received as the study did not have sufficient resources to use independent blinded assessors for clinical assessments. People in the standard treatment group (the non-surgery group) could have surgery after one year if their treatment was still not adequately effective.

 

What were the basic results?

One year after surgery, people who received DBS in addition to best medical treatment showed greater improvement in their quality of life than those who received best medical treatment alone. The DBS group improved by 5 points on the PDQ-39 scale and the medical group by only 0.3 points.

 The quality of life questionnaire assessed different areas of life and showed that people who received DBS had greater improvements in mobility, activities of daily living and bodily discomfort. The difference between the groups was 8.9 points for mobility, 12.4 points for activities of daily living, and 7.5 points for bodily discomfort. Participants who received DBS also showed greater improvements in clinically assessed overall functioning at one year than participants receiving medication alone. Participants who received DBS had reduced their drug dose by about 34% compared with the medical treatment group.

Just under one in five people who received DBS had serious adverse effects associated with their surgery (19%), and one patient died from bleeding during surgery. Similar proportions of patients had side effects of their medical treatment in both groups (11% with DBS plus medical treatment, and 7% with medical treatment alone).

 

How did the researchers interpret the results?

The researchers concluded that one year after the study began, treatment that combined surgery and best medical therapy “improved patient self-reported quality of life more than best medical therapy alone in patients with advanced Parkinson’s disease”.

They also say that the improvements seen were clinically meaningful, but that the risks associated with DBS surgery may warrant only offering the surgery to those people most likely to benefit from it.

 

Conclusion

This study used a robust design to assess the effects of deep brain stimulation (DBS) on quality of life in people with Parkinson’s disease that had not responded adequately to medical treatment. Points to note include:

• Blinding participants and researchers to the treatment received was not possible, so participants’ ratings of their quality of life may have been affected if they had pre-existing expectations of DBS or if they were disappointed not to have received DBS.
• The trial has so far collected and reported one year’s worth of data. The researchers are continuing to collect information on the patients’ outcomes so that the longer-term effects of DBS can be studied.
• The researchers suggest that the group of patients treated were representative of those who would be offered surgery at neuroscience centres in the UK.
• A questionnaire was given to participants in the DBS group about surgery-related adverse effects six months after surgery, but a similar questionnaire was not given to the medical treatment only group. Therefore, adverse effects in the latter group could have been missed. The researchers also note that they did not record adverse effects that were not serious enough to cause a patient to be admitted to hospital or to extend their stay in hospital.
• People who received DBS continued to receive medical therapy, although the drug dose could be reduced in many cases. Therefore, news reports that “brain surgery is more effective than medication” or “implants have given us our life back” should not be misinterpreted to mean that DBS is a complete cure or that a person will no longer need any form of drug treatment. People should also be aware that all surgical procedures are associated with some degree of risk and this treatment would not be suitable for everyone. Advances and developments in the DBS technique are likely to continue.

Overall, the results suggest that combining DBS with the best medical therapy can improve quality of life more than medical treatment alone in people with Parkinson’s disease that has not responded adequately to medical treatment.

Links To The Headlines

Brain ‘pacemaker’ surgery hope. BBC news, April 29 2010

Brain surgery hope for Parkinson’s cases: Implants have given us our life back say first patients. Daily Mail, April 29 2010

Brain ‘pacemaker’ fights Parkinson’s. The Independent, April 29 2010

Links To Science

Williams A, Gill S, Varma T et al. Deep brain stimulation plus best medical therapy versus best medical therapy alone for advanced Parkinson’s disease (PD SURG trial): a randomised, open-label trial. The Lancet Neurology, [Early Online Publication], April 29 2010

“Drinking too much pop can speed up the ageing process,” the Daily Mail reported. It said research has found that phosphate, a chemical that gives many drinks their tangy taste, can accelerate ageing.

This study was in mice that were genetically engineered to age prematurely. Although animal studies can provide information on how biological processes work, these findings may or may not be relevant to the human body. It is a big leap from these findings to the suggestion that fizzy drinks containing phosphates could cause premature ageing.

The effect of excess phosphate on health is important enough to justify further research. However, it is unclear if the levels of phosphate in fizzy drinks are enough to affect health. At present, the high sugar and calorie content of these drinks would seem to be a more compelling reason for limiting their intake.

 

Where did the story come from?

This research was carried out by Mutsuko Ohnishi and M Shawkat Razzaque from the Harvard School of Dental Medicine, USA, and Nagasaki University Graduate School of Biomedical Sciences, Japan. The study was funded by the National Institute of Diabetes and Digestive and Kidney Disease. The work was published in the peer-reviewed scientific journal Federation of American Societies for Experimental Biology (FASEB).

 

What kind of research was this?

This animal study investigated factors potentially involved in the ageing process and aimed to identify possible therapeutic targets for slowing down this process. Of particular interest was the breakdown of phosphate in the body, as phosphate is widely distributed throughout the body and is involved in many cellular processes. The researchers say that problems with phosphate breakdown have been noted in several heart, kidney and skeletal diseases. However, whether or not phosphate has a role in the ageing process has never been firmly established.

 

What did the research involve?

The researchers used genetically engineered “klotho-knockout” mice. These mice have a short lifespan and show many biochemical and physical signs that are consistent with premature ageing. These include curvature of the spine and brittle bones, uncoordinated movement, muscle wasting, lung complaints and generalised weakness of several body tissues and organs.

Phosphate absorption in the body is mainly controlled through sodium-phosphate transporter (NaPi2a) channels. These are found in the large intestine, where they absorb phosphate from the gut, and in the kidney, where they reabsorb phosphate and prevent it from being lost in urine. In klotho-knockout mice, the activity of the sodium-phosphate transporter (NaPi2a) channels in the kidney is increased, resulting in their bodies having a lifelong high level of phosphate.

The researchers adapted these mice further, creating a mouse that lacked this transporter (klotho-knockout/NaPi2a-knockout mice). In theory, this mouse would retain its properties of premature ageing, but would also have reduced phosphate levels in the body.

The researchers fed one group of klotho-knockout mice and klotho-knockout/NaPi2a-knockout mice a normal diet. Another group of the two types of genetically engineered mice was fed a high-phosphate diet.

 

What were the basic results?

The researchers found that, on the normal diet, the klotho-knockout/NaPi2a-knockout mice showed less evidence of premature ageing than the klotho-knockout mice. The mice regained reproductive ability and had improved body weight, reduced wasting and weakness of body organs, and overall prolonged survival. Conversely, in klotho-knockout/NaPi2a-knockout mice that were fed a high-phosphate diet, the signs of premature ageing reappeared.

 

How did the researchers interpret the results?

The researchers concluded that high phosphate levels are the main cause of ageing in mice that are genetically engineered to age prematurely.

 

Conclusion

This animal study investigated the possible role that levels of phosphate in the body play in the ageing process. Problems with phosphate breakdown have previously been noted in several heart, kidney and skeletal diseases.

The study looked at a group of mice genetically engineered to age prematurely, and assessed the effect of removing a phosphate transporter in the kidney (by further genetic alteration). As expected, these mice had reduced phosphate levels in the body and were free of the signs of premature ageing that the other mice had (for example, they retained fertility and had less skeletal and muscle wasting). Giving these mice a high-phosphate diet raised their phosphate levels, resulting in changes associated with ageing.

While animal studies can provide information on how biological processes work, these findings in mice, which were genetically engineered to prematurely age, may or may not be relevant to the human body. It is a big leap from these findings to the suggestions that fizzy drinks containing phosphates can cause premature ageing.

The effect of excess phosphate on health is important enough to justify further research. However, it is unclear whether the levels of phosphate in fizzy drinks are enough to affect health. At present, the high sugar and calorie content of these drinks would seem to be a more compelling reason for limiting their intake.

Links To The Headlines

Drinking too much pop can speed up the ageing process. Daily Mail, April 28 2010

Links To Science

Ohnishi M and Shawkat Razzaque M. Dietary and genetic evidence for phosphate toxicity accelerating mammalian aging. The FASEB journal, [Published online] April 23 2010