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Dairy Intake And Semen Quality Among Men Attending A Fertility Clinic

Discussion in 'Scientific Studies' started by Nicolas Noyola, May 8, 2018.

  1. Nicolas Noyola

    Nicolas Noyola Member

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    Dairy intake and semen quality among men attending a fertility clinic
    Dairy intake and semen quality among men attending a fertility clinic
    Low-fat dairy intake was positively related to sperm concentration and progressive motility. On average, men in the highest quartile of intake (1.22–3.54 servings/day) had 33% (95% confidence interval (CI) 1, 55) higher sperm concentration and 9.3 (95%CI 1.4, 17.2) percentage units higher sperm motility than men in the lowest quartile of intake (≤0.28 servings/day). These associations were primarily explained by intake of low-fat milk. The corresponding results for low-fat milk were 30% (95%CI 1,51) higher sperm concentration and 8.7 (95%CI 3.0, 14.4) percentage units higher sperm motility. Cheese intake was associated with lower sperm concentration among ever smokers. In this group, men in the highest tertile of intake (0.82–2.43 servings/day) had 53.2% (95%CI 9.7, 75.7) lower sperm concentration than men in the lowest tertile of cheese intake (<0.43 servings/day).

    #2 Study​
    Dairy food intake in relation to semen quality and reproductive hormone levels among physically active young men
    Dairy food intake in relation to semen quality and reproductive hormone levels among physically active young men

    Total dairy food intake was inversely related to sperm morphology (P-trend = 0.004). This association was mostly driven by intake of full-fat dairy foods. The adjusted difference (95% confidence interval) in normal sperm morphology percent was −3.2% (−4.5 to −1.8) between men in the upper half and those in the lower half of full-fat dairy intake (P < 0.0001), while the equivalent contrast for low-fat dairy intake was less pronounced [−1.3% (−2.7 to −0.07; P= 0.06)]. Full-fat dairy intake was also associated with significantly lower percent progressively motile sperm (P= 0.05).

    Both studies concluded that full-fat dairy intake harms fertility. Now I was operating under the assumption that skim-milk contains less estrogen than whole-milk, but the user Travis conducted an interesting and intelligent analysis of the hormonal contents of the various milk types: The Travis Corner

    [​IMG]

    he also compared the ratios of androgens to estrogens and concluded that whole-milk actually has a much better ratio than skim-milk. So whole-milk should be more pro-androgenic and pro-fertility than skim, but this study apparently turns that idea on its head. The first-study doesn't really offer any condemnation of low-fat dairy, only full-fat, but in the second study it seems that intake of dairy of any kind reduces sperm count. The second study also handily measures hormonal levels and compares it with dairy intake quartiles (Study 2, Table IV). There was basically little correlation with dairy intake and any sort of hormone, except for FSH, where levels were 27% and 26% higher among the 4th quartile for full-fat and total dairy-intake respectively compared to the 1st quartile.

    There was an association between higher intake of total dairy foods with higher FSH levels (P-trend = 0.05). This association was stronger among men with at least one semen analysis abnormality (n= 50; P-trend = 0.003) than among men with no semen analysis abnormality (n= 139; P-trend = 0.61, Fig. 2).

    Anyways given that there are lots of doubts regarding milk and estrogen and whatnot, I decided I would post these studies here to stimulate some (hopefully) illuminating discussion. Thoughts? ​
     
  2. Mossy

    Mossy Member

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    Greater minds than me can provided better answers, but I can opine that there are many variables, first and foremost that being the objectivity, or subjectivity, of the researchers. Did they have a narrative they were attempting to compliment and/or uphold. Granted, they may be 100% correct; but, as you've pointed out, another scientist, @Travis, has shown opposing results.

    One thing I'm convinced of, considering science--or anything else these days--true objectivity is a rarity, and most "research" deserves scrutiny and to be put to additional testing and proper peer review.
     
  3. jyb

    jyb Member

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    On a related note, consider the fact that dairy is the food group the most contaminated with phthalates (plastics), which are blamed for lowering semen quality.
     
  4. OP
    Nicolas Noyola

    Nicolas Noyola Member

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    this is one of the hypotheses of the authors of the study actually, which they evidence by the fact that the highest quartiles of milk-drinkers had elevated FSH levels and that exposure to chemicals like pesticides (they mention organophosphates) has been linked to high FSH. Additionally, I looked up some studies regarding FSH and fertility, semen, and scrotal/testis size, with the general correlation being negative between FSH and all those variables.
     
  5. Sobieski

    Sobieski Member

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    Good news for me then. My FSH is very low. In an email Peat even said to me that FSH and LH are best to be low with high androgens.
     
  6. Mossy

    Mossy Member

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    Interesting. I could more readily believe it was the plastic that was the contributor to the poor fertility.

    I wonder if the waxed/treated square cardboard containers would be less of an issue, compared to the plastic. Obviously, glass would be ideal, but the milk is always more expensive in those.
     
  7. Waremu

    Waremu Member

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    Lucky for me, IF it is due to mostly plastics, as I get raw milk that comes in class jars. That said, we don’t know how much of these negative effects were attributed to plastics IF it was related to plastics in some way. For all we know, unless there is other evidence, the plastics may only contribute to 30% or 50%, for example. So this does still somewhat trouble me. I wish they did a study like this in raw milk or organic normal milk not sold in plastic.
     
  8. Travis

    Travis Member

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    Perhaps we should consider for a moment what could be a more potent sperm growth factor.

    The polyamines spermine and spermidine were eponymously named for their presence in sperm. These two polyamines are powerful growth agents shown to: bind dNA, induce a transition from the righthanded B configuration to the lefthanded Z configuration, and enhance dNA replication rates during PCR. Because polyamines don't need anything besides dNA and -mRNA polymerase, they operate on a more fundamental level than do steroids. Androgens need a receptor to replicate dNA in addition to RNA polymerase, but polyamines don't even need one of those. In fact, one of the functions of androgens is to increase ornithine decarboxylase expression (which then makes polyamines). The powerful ability of spermine to induce dNA replication perfectly explains its presence in the sperm cell, and also how it induces replication in the egg (the polyamines unpack the dNA from the core histones, allowing transcription of segments that wouldn't occur otherwise).

    Although there are only slight changes in the methionine (protein) concentration between skim and full-fat milk, we also should realize that this was an observational study. Even though skimming the fat off of milk only increases the protein concentration by about 8%, doing this also reduces the energy content by 44%—meaning those drinking skim milk would consume more protein from other foods (on an iso-caloric diet).

    In boars: protein has been found been found to increase volume by 35%, yet this had no effect on sperm motility. There had been no difference in testosterone levels, but the 'concentration of estradiol-17β was greater in boars fed the control diet than in boars fed the low-protein diet (582 vs 202 pg/mL, respectively; P < .08).' I think this could mean that stearic acid could potentially induce estradiol synthesis by creating the need for stearoyl–CoA desaturase (to oleic acid).

    But what effects sperm motility if not 17β-estradiol or methionine? Well . . . if I were to guess I'd say the intra-cellular Ca²⁺/Mg²⁺ ratio. As far as I'm concerned, calcium is the fundamental and essentially non-reducible catalyst of muscle contraction. Sperm cells do have tiny muscles, obviously, and these would be calcium-dependent.


    'Other factors which have been shown to stimulate sperm cyclase include high levels of spermine (Shah et al., 1975, Casillas et al., 1980) and calcium. With regard to calcium, the activation of cauda epididymal hamster sperm can be initiated by external calcium. In fact there is a dose-dependent increase in both motility and cAMP content produced by external calcium at concentrations ranging from 0.1 to 3.0 mM (Morton et al., 1974). Hyne and Garbers (1979a) have shown that guinea pig sperm adenylyl cyclase is stimulated by calcium even in the presence of manganese. Finally, Watkins et al. (1978) have shown that factors from sea urchin eggs that stimulate sperm adenylyl cyclase do so in a calcium-dependent manner.'

    'As mentioned above, the first indications that cAMP may be involved in sperm motility resulted from experiments concerning the stimulatory effects of compounds such as caffeine and theophyiline on the motility of sperm. These compounds were known to inhibit cyclic nucleotide phosphodiesterase (Butcher and Sutherland, 1962; Beavo et al., 1970) and were indeed shown to increase cAMP concentrations in sperm (Garbers et al., 1971b, 1973b; Hoskins et al., 1975). However, compounds like caffeine and theophylline were known to affect other enzymes in addition to phosphodiesterase (Robison et al., 1971; Slaughter et al., 1982), so it could not be conclusively demonstrated that these com- pounds were stimulating motility directly by increasing cAMP content.'

    '...in relation to capacitation and the acrosome reaction, Hyne and Garbers (1979b) found that guinea pig spermatozoa, capacitated in both the presence and absence of calcium showed an increase in cAMP associated with the acrosome reaction. In sperm capacitated in the absence of calcium, subsequent addition of calcium brought about a rapid increase in cAMP content which was followed within minutes by the acrosome reaction. Cornett and Meizel (1978) demonstrated that hamster spermatozoa treated with a and 3 agonists showed typical capacitation-associated “activated” motility coincident with the acrosome reaction. Beta-agonists, such as epinephrine and isoproterenol, act primarily via stimulation of cAMP levels, whereas a-agonists are proposed stimulators of calcium flux (Lefkowitz, 1976). It would appear that the effects of the 13-agonists on motility would be via stimulation of cAMP and the a-agonists via calcium. Such conclusions would be consistent with the results of Hyne and Garbers (1979b) described above. How calcium and cAMP may interplay in these processes is discussed later in this review. As mentioned earlier, the use of phosphodi- esterase inhibitors yielded the first clues that cAMP may play a role in the regulation of sperm motility.'

    'The fact that phosphodiesterase inhibitors show the most pronounced effect on motility of poorly motile cells, and that under optimal metabolic conditions cAMP levels are high, suggests a close coupling between metabolic state, motility and cAMP levels. Since phosphodiesterase inhibitors produce an increase in sperm cAMP content without affecting motility of already highly active cells, cAMP levels in highly motile cells are likely to be sufficiently high to completely activate the subsequent steps of the cAMP cascade, i.e., cAMP-depen- dent protein kinase activation and stimulated protein phosphorylation.'

    Intracellular calcium is controlled primarily through membrane receptors. These receptors are coupled to enzymes which either influencing intracellular cAMP levels or phosphoinositide levels (the latter being a well-established, high-affinity calcium chelator). Besides magnesium, which displaces calcium, intracellular Ca²⁺ is most well-correlated with the concentrations of these two 'secondary messengers.' Cyclic AMP is formed at the expense of ATP, which is the high-affinity magnesium-chelator). Thus: anything which inhibits phosphodiesterase (i.e. caffeine), activates phospholipase C (i.e prostaglandin E), or activates adenylate cyclase (i.e. N-methyl-D-aspartate) should increase intracellular calcium; this intracellular calcium, in turn, should increase excitability. I would expect sperm motility to be a function of intracellular calcium and also the things which increase it—e.g. dopamine, epinephrine, caffeine—while being negatively-correlated with magnesium.

     
  9. Mossy

    Mossy Member

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    Thanks Travis.

    This is going to be a shot in the dark, as your comment triggered something way back in my mental database. About 4 years ago, on my blood test, my estradiol levels were showing what a Life Extension article was categorizing as low, and outside the optimal "balanced quintile...serum estradiol levels between 21.80 and 30.11 pg/mL.". Did I interpret this comment correctly, that full-fact milk could increase estradiol production?

    I realize I my have gotten this wrong, but I'm willing to put it out there just in case there is something to it, that drinking full-fat milk (or is it the other way around) could put me in the "balanced quintile"--if there is any truth to this perspective by Life Extension.

    So, if I've gleaned correctly, it seems the moral of the story is to get the "intra-cellular Ca²⁺/Mg²⁺ ratio" right.
     
  10. jyb

    jyb Member

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    Dairy is unusual - studies show that the contamination is not due to the store packaging. It's just as high for organic milk in glass for the products that were sampled. The source of the contamination is unknown, but we can speculate it is due the milking tubes or what stores the warm milk.
     
  11. Mossy

    Mossy Member

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    Ah, interesting. Never thought of that. So, even if you purchase raw milk, in glass, if the milking or storage process uses plastic, you're still susceptible.
     
  12. Travis

    Travis Member

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    Well . . . the event of estradiol binding to its intracellular receptor has been consistently shown to induce the transcription of desaturase enzymes. Following from this should be an increase in cell membrane fluidity and glucose flux, both of which are correlated with increased cellular proliferation. A diet high in stearic acid could be sensed by the body, somehow, and this could perhaps lead to the induction of aromatase to increase membrane fluidity (countering stearic acid).

    But there is little use on speculating any further since this can be known simply by reading studies.. . [reading] . ..I did find this one showing the effects of estradiol on fatty acid triglycerides:


    'Less research has been published on the effects of estradiol. In a study on the relationship between estradiol and phospholipids (3, 4), we showed that estradiol has different effects on the fatty acid composition of the various lipoprotein classes. Here we report the results of a detailed investigation of the effects of estradiol on serum levels of phospholipids, triglycerides, cholesterol (free, total and esteritied) and of their fatty acid composition, in normal, castrated and estradiol treated rats.' ―Cinci

    'They received water and a standard diet ad libitum. At the beginning of the experiments, the rats were divided into three groups: the first group was sham-operated and used as control; the second was castrated under ether. The rats of the third group were also castrated and one month after castration, injected i.m once a week, with different doses [10 μg/rat or 1 mg/rat], of estradiol cypionate dissolved in peanut oil. Control and group 2 rats were injected with peanut oil only. All rats consumed the same quantity of food:' ―Cinci


    'Total lipids were extracted from 1 ml of serum, according to Folch et al. (5), with 24 ml chloroform/methanol mixture (2∶1).' ―Cinci


    'The fatty acid methyl esters were identified by comparison of retention times with standards and the mass distribution was calculated by gas liquid chromatography (GLC) using C16:0, Cl6:1, C18:0, C18:1, C18:2, C18:3 and C20:4 as internal standards.' ―Cinci


    lipids.png

    The table reporting the change in the stearate∶oleate ratio is even more revealing:

    lipids2.png
    So the fact that estradiol decreases the 18∶0/18∶1 ratio—or increases the inverse ratio—is very consistent and reliable; I have seen no exception to this effect. The Δ⁹-desaturase enzyme in question has been shown to be induced by estradiol on the enzyme level (Western blot), on the nucleic acid level (microarray and real-time PCR), and even on the lipid level (above).

    The question is then: Does modifying the dietary 18∶0/18∶1 ratio induce a corresponding change in estradiol levels?

    (Perhaps we need to read some studies on the high-oleic acid, and high-oleamide Italians?)
     
  13. Mossy

    Mossy Member

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    I appreciate the reply. As always, your answers are extensive and challenging, but worth the effort--thank you.
     
  14. sladerunner69

    sladerunner69 Member

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    So is the packaging of milk a concern? I would be very surprised if Dr Peat had not concerned this in his personal tendency to drink a gallon of milk per day. If plastics were being leached, I would suspect that one would notice a gallon of milk per day having a negative effect ton mood and personality.
     
  15. RMJ

    RMJ Member

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  16. Mossy

    Mossy Member

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    I think the discussion drifted towards the plastic aspect, as an alternative to the milk itself being the cause of lowering fertility and androgens: "...in the second study it seems that intake of dairy of any kind reduces sperm count."
     
  17. sladerunner69

    sladerunner69 Member

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    Milk is such a central staple of peatland, I would not think the discussion of milk packaging or otherwise ill effects to be swept aside without a more thorough investigation.
     
  18. Mossy

    Mossy Member

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    I agree.

    Until more studies and research show the consistency of anti-fertility and androgen effects from milk, I think blaming the milk itself has to be taken with a Peat-pun--a grain of salt. As for the plastic(s) being the cause, maybe I've drank the anti-plastics Kool-aid, but that seems to be more viable. The most concerning aspect to me, as @jyb noted, is that the problem could be the plastic tubing/containers used in milking/processing; meaning, storing the end-product in glass, would not counter those original negative effects--though, maybe it could reduce further issues.
     
  19. Arnold Grape

    Arnold Grape Member

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    Milk tastes gross in plastic.
     
  20. Waremu

    Waremu Member

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    The problem is, as stated already, the tubes/processing and not the milk issue itself is pure speculation at this point, unless such evidence is found. Even if the tubes/filtration they use is considered, we need to ask: is it enough to be the cause, since the milk isn't sitting long term in the tubes. From what I have read, it seems that the milk is processed relatively quickly though the tubes/filtration process, so we would need to ask if milk is moving that quickly, would it be enough to cause this, as well. Regardless, whether it is the milk itself or the filtration/plastic, the vast majority of milk is processed in similar ways, though I would like to see more evidence regarding milk and sperm count, I think there is at least enough evidence which raises concern, and so the effect for me is serious enough to seriously consider drinking less commercial milk and trying to fill my other half of calcium in with green broth, etc. I may even experiment going milk free for the time being. As long as I get enough calcium/magnesium elsewhere, I don't see it as a huge loss if I do ditch it for the time being. Milk makes Peating much easier, but I don't see it as being essential to Peating either as long as the minerals are covered elsewhere. Whether milk does or does not truly lower sperm count, I see it as being better safe than sorry, until more evidence comes forth. And if more evidence comes forth showing milk doesn't, adding milk back in won't be anywhere near as bad as taking it out after waiting for more such evidence.
     
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