Monday, July 22, 2013
High intake of saturated fat & sperm quality in Danish men
Below are some excerpts from a skeptical writer. I can only echo her point that sperm motility is the key factor in fertilization and the numbers show no effect of fat on motility
“Eating a fatty diet could reduce a man’s sperm count by 40%” said the Daily Mail – enough to put every man off his bacon & egg. The Globe and Mail warned similarly: “Eating too much saturated fat may decrease sperm counts.”
The headlines came from a study published in the American Journal of Clinical Nutrition.” High dietary intake of saturated fat is associated with reduced semen quality among 701 young Danish men from the general population.” Unfortunately only the abstract is on free view – I’ve got hold of the full article to see what it’s all about.
As the article title confirms – the study involved 701 Danish men who signed up for military training between April 2008 and June 2010. The men “delivered a semen sample, underwent a physical examination, and answered a questionnaire comprising a quantitative food-frequency questionnaire to assess food and nutrient intakes.” The food questionnaire was intended to review the three months prior to the military training sign up appointment.
The full article states (in the introduction) “We therefore examined the associations between dietary fat intakes and semen quality among 701 young Danish men from the general population, hypothesizing that a high intake of saturated fat is associated with reduced semen quality.” So, the researchers hypothesised that saturated fat intake is associated with reduced semen quality before doing the study. As Einstein said, if you know what you’re looking for, it ain’t research!
The conclusions of the study were: “…men in the highest quartile of saturated fat intake had a 38% (95% CI: 0.1%, 61%) lower sperm concentration and a 41% (95% CI: 4%, 64%) lower total sperm count than did men in the lowest quartile. No association between semen quality and intake of other types of fat was found.”
Table 2 is interesting. This has semen volume, sperm concentration, total sperm count and motile sperm (the latter gives an indication of the quality of the sperm – their ability to move effectively towards an egg) against the different quartiles for total fat, SFA, MUFA, PUFA and even gets down to omega-3 and omega-6 essential fatty acids. Let’s just take the part of the table for SFA vs the sperm measurements:
This tells me that the ‘best’ intake of saturated fat for semen volume, sperm concentration, total sperm count and motile sperm is 11.2-13.27% of dietary energy (a bit precise, but that’s what it suggests). There’s barely any difference between the third and fourth quartiles and the second quartile is ‘better’ than the first. This is notwithstanding all the variables stacked against the quartiles as they go up from 1 to 4 for everything else – alcohol, smoking, STD’s, age, being underweight etc.
Table 3 tries to “take into account confounders”. However, it only tries to take into account BMI, alcohol consumption, smoking and the period of abstinence before the sample. It doesn’t appear to take into account the nearly three times higher incidence of STDs and there being more men in Q4 over 20 than in Q1. Even if all attempted confounders have been perfectly accounted for (and I can’t see how, from the SFA data in Table 2 being unremarkable and the different attributes in Table 1 being significant), surely the difference in age in Q4 and the highly significant difference in the incidence of STDs could alone explain any difference in sperm quality? (Again – not that the difference in sperm quality in Table 2 is much to get excited about).
Table 3 also no longer mentions motility – that’s the statistic to get excited about if you’re trying to conceive – why was this dropped? Did it not give ‘the right’ answer?
It also makes no sense to claim an association with saturated fat and not total fat or any other fat. Saturated fat cannot be eaten alone. Every single food on the planet that contains saturated fat also contains monounsaturated fat and polyunsaturated fat – there are no exceptions. The extracted numbers from Table 1 confirm that total fat, monounsaturated fat and polyunsaturated fat all increased from Quartile 1 to Quartile 4 and yet we are led to believe that only saturated fat is associated with sperm concentration and sperm count.
Not only is this not plausible, no plausible mechanism is offered for any possible explanation for proposed association throughout the article. How can saturated fat intake (alone from other fat intake and total fat intake) impact sperm concentration and sperm count?
If the period of abstinence tells us anything, a much more interesting headline could have been “Men who eat more saturated fat have sex more frequently!”
SOURCE
Statins risk for women: Taking cholesterol-lowering drug for more than ten years 'doubles chances of the most common breast cancer'
The statin religion is unraveling at long last
Women who take statins for more than a decade face double the risk of contracting the most common type of breast cancer.
Alarming findings raise new concerns over the long-term safety of a widely prescribed medicine in the UK.
Previous studies have suggested the cholesterol-lowering drugs, used by an estimated eight million men and women, can reduce the risk of certain cancers – including the breast form of the disease.
However, most research looked at patients who had only been on them for five years or less.
The latest findings identified invasive ductal carcinoma (IDC) which starts in the ducts of the breast before spreading inwards. It accounts for around seven out of ten breast cancer cases.
The experts at the Fred Hutchinson Cancer Research Centre in Seattle, US, also found the chances of getting invasive lobular carcinoma, which accounts for ten to 15 per cent of breast cancers, went up almost 2.5 times in some women on statins long-term.
Around 48,000 women in Britain are diagnosed with breast cancer each year, equal to around 130 a day. A woman has a one in nine chance of developing the disease at some point in her life.
The reasons why the anti-cholesterol pills might stimulate cancer growth are unclear.
The researchers said one explanation may be that statins affect hormone regulation in the body, especially as the study found women on the drugs were significantly more likely to suffer cancers driven by the hormone oestrogen.
They said it’s possible that while short-term use does appear to have a protective effect against breast cancer, in the long-run statins may damage certain chemical pathways that lead to growth of tumours.
The report found: ‘As more women are taking them and for longer durations it is possible we will observe effects that prior studies could not detect.’
Last night, leading UK cancer bodies called for urgent research to clarify the risks to women.
But they urged patients on statins not to stop taking them without consulting their GP.
Sally Greenbrook, from the charity Breakthrough Breast Cancer, said: ‘Any study suggesting a potential link between statins and breast cancer risk should not be taken lightly. But these drugs are extremely effective at reducing the risk of cardiovascular disease.’
Jessica Harris, of Cancer Research UK, said: ‘There’s been a huge amount of research into the link between statins and cancer. ‘But so far there’s no conclusive answer, with some studies showing a reduced risk, some no link, and others showing a raised risk.’
Statins have also emerged as a major weapon against heart disease in the last 20 years.
The latest research, published in the journal Cancer Epidemiology Biomarkers and Prevention, examined how long-term statin use affected breast cancer risk in women aged between 55 and 74.
The researchers studied just under 2,000 women diagnosed with either IDC or ILC between 2000 and 2008 and a separate group of 902 women of a similar age profile but who were free of cancer.
Around 370 men a year in the UK are diagnosed with breast cancer – but the latest research did not investigate the cancer risk of men taking statins.
SOURCE
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