Guest guest Posted August 7, 2003 Report Share Posted August 7, 2003 --- In , Ian Goddard <iamgoddard@y...> wrote: > > FINDINGS MAY SUPPORT SOY-DEMENTIA CORRELATION IN MEN > > © 08/06/03 - Ian Goddard > > In April 2000, Lon White and others reported a dose-dependent positive > correlation between tofu consumption and brain atrophy in a large > sample of men over several decades. [1] While correlation does not > prove causation, study size and duration along with the robust > dose-dependent relationship caused me, even as a vegetarian, to avoid > tofu and other soy products. > ................_______________________________________________________ ________________ > [1] White et al: " In this population, higher midlife tofu consumption > was independently associated with indicators of cognitive impairment > and brain atrophy in late life. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=10763906 & dopt=Abstract > > [2] Goddard (scroll to): " Is There Reason to Believe Tofu May Cause > Brain Atrophy? " http://iangoddard.net/soy.htm > > [3] Exp Neurol (Sep 2002): " Neurotrophic factors have long been known > to promote neuronal survival and differentiation. " > http://www.neuro.mpg.de/research/csn/bdnf_ltp > > [4] J Neurochem (Sep 2002): " These findings suggest that BDNF plays an > important role in the regulation of the basal level of neurogenesis in > dentate gyrus of adult mice [...]. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=12354284 & dopt=Abstract > > [5] Endocrinology (Jun 2003): " Recent studies have shown that DR > [dietary restriction] stimulates the production of brain-derived > neurotrophic factor (BDNF) in brain cells, which may mediate > neuroprotective and neurogenic actions of DR. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=12746306 & dopt=Abstract > > [6] Arch Gen Psychiatry (Jul 1997): " stress can decrease the > expression of brain-derived neurotrophic factor and lead to atrophy of > these same populations of stress-vulnerable hippocampal neurons. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=9236543 & dopt=Abstract > > [7] Brain Res Mol Brain Res (Oct 3, 1997): " a reduction in BDNF mRNA > expression has been observed in human post-mortem Alzheimer's disease > hippocampi. [...] These results support and extend previous findings > that BDNF mRNA is reduced in the human Alzheimer's disease hippocampus > and temporal cortex, and suggest that loss of BDNF may contribute to > the progressive atrophy of neurons in Alzheimer's disease. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=9387865 & dopt=Abstract > > [8] Neurosci Lett (Feb 27, 2003): " significant reductions were found > in brain-derived neurotrophic factor (BDNF) mRNA expression in the CA3 > and CA4 region of the hippocampus and in the cerebral cortex in the > [male] rats fed the diet containing phytoestrogens, compared with > those on the soya-free diet. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=12566171 & dopt=Abstract > > [9] Neurosci Lett (Feb 1999): " soy phytoestrogens significantly > increased the mRNA levels of BDNF [...in] female rats. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=10081916 & dopt=Abstract > > [10] Neurotoxicol Teratol (Jan-Feb 2002): " when learning and memory > parameters were examined in a radial arm maze testing visual-spatial > memory (VSM), the diet treatments significantly changed the typical > sexually dimorphic pattern of VSM. Specifically, adult Phyto-rich fed > females outperformed Phyto-free fed females, while in males on the > same diets, the opposite pattern of maze performance was observed. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=11836067 & dopt=Abstract > > [11] BMC Neurosci (2001 2(1):20): " Female rats receiving lifelong > exposure to a high-phytoestrogen containing diet (Phyto-600) acquired > the maze faster than females fed a phytoestrogen-free diet > (Phyto-free); in males the opposite diet effect was identified. [...] > These findings suggest that dietary soy derived phytoestrogens can > influence learning and memory and alter the expression of proteins > involved in neural protection and inflammation in rats. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=11801187 & dopt=Abstract > > [12] BMC Neurosis (2001 2(1):21): " When a diet change was initiated in > adulthood, control phytoestrogen-rich fed females outperformed control > females switched to a phytoestrogen-free diet. Whereas, in control > males the opposite diet effect was identified. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=11801188 & dopt=Abstract > > [13] Neurosci Lett (May 15, 2003): " This study is the first to show > that lifelong consumption of dietary phytoestrogens alters the HPA > stress response in male rats. " > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=12727319 & dopt=Abstract > > [14] Dementia: http://okinawaprogram.com/images/dem.gif > > [15] Soy intake: http://okinawaprogram.com/images/ment.gif > > Some alternative views on soy: > http://www.soyonlineservice.co.nz > http://www.healingcrow.com/soy/soy.html Hi All, Saul appears to describe evidence based on animal models for the testing using unknown concentrations of phytochemicals relative to human consumption and in animals that may not be appropriate to model human conditions. See the bottom, since I believe that mortality is the bottom line. Cheers, Al. Am J Epidemiol. 2002 Nov 1;156(9):824-31. Soy and fish oil intake and mortality in a Japanese community. The relation between intake of fish and soy products and subsequent all-cause and cause-specific mortality was examined in a cohort of 13,355 male and 15,724 female residents of Takayama, Gifu, Japan. A diet that included soy and fish intake was assessed in 1992 by using a validated semiquantitative food frequency questionnaire. .... For men, the highest compared with the lowest quintile of total soy product intake was marginally significantly inversely associated with total mortality after adjustment for total energy and nondietary covariates (hazard ratio = 0.83, 95% confidence interval: 0.69, 1.01; p for trend = 0.07). After adjustment for nondietary covariates, a decreased hazard ratio for the highest compared with the lowest quintile of total soy product intake was also observed for women (hazard ratio = 0.83, 95% confidence interval: 0.68, 1.02; p for trend = 0.04). Additional adjustment for dietary factors significantly associated with total mortality did not attenuate these associations. For women but not for men, n-3 fatty acids from fish were significantly inversely associated with total mortality. Results showed that soy intake may have moderate but beneficial effects on total mortality. PMID: 12397000 [PubMed - indexed for MEDLINE] Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2003 Report Share Posted August 7, 2003 Ian wrote: I contacted Lon White, lead researcher in the tofu study to ask some questions. I asked him about the statistical significance of the findings in the study. He informed me that there were four major endpoints in the study: 1. cognitive impairment of men (number of men=3734) 2. cognitive impairment of sample of wives (n=502) 3. brain atrophy by weight of men who died (n=290) 4. brain atrophy by volume measured via MRI (n=574) The probability (p) value was less than .05 (significant) for a correlation between each endpoint and tofu intake (there was no significant correlation for other foods). In some cases the p value is less than .001 (if the p value is more than .05, it's not significant, if it's .05 or less, it's significant). Here's what this means: IF p = .05 there's 95% chance the correlation is true IF p = .01 there's 99% chance the correlation is true IF p = .001 there's 99.9% chance the correlation is true So the correlation between the four endpoints listed above and tofu consumption had an over 95% probably of being true, with a probability of truth as high as 99.9%. Of course this cannot be read as proof that tofu causes those problems, but at the least it signals the need for further investigation. What is perhaps most significant is that Dr White informed me that there is a dose-dependent relationship between tofu consumption and the endpoints, ie, the more tofu was eaten, the more impairment and/or atrophy is found. The odds that such findings would be chance are extremely low! Hi Ian & ALL: What caught my eye is this dose-dependent factor! Since you are an expert on this topic of soy, could you agree that if one ate soy only occasionally, perhaps once per week a glass of soy milk or 1/4 tub of tofu, that one's brain is far less likely to be affected by eating soy? What would be your definition of low risk & time to eat such a quantity of soy noted above? Weekly, bi-weekly, monthly? Going on the idea of moderation, moderation, & dose-dependent there might be a low-risk solution to just eat soy occasionally? Also, since the risk seems related to Genistein are there certain types of soy products you know of that have much less of this substance? Hey, even MR still eats some soy, as it's in one of his recipes, so he must consider occasional soy consumption a risk worth taking too. Your comments & ideas are most welcome. Also, Al Pater, if you read this, what do you think the research shows supporting or contradicting this "danger soy" theory? Thanks! numi .. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2003 Report Share Posted August 7, 2003 Ian, Thanks VERY much for getting that information from Dr. White. Last night I was concerned about the findings, but feel better now that I see how large the sample is. The critical thing for interpreting a finding like this is the effect size, or the magnitude of the correlation. Luckily, with 3734 subjects in the study, correlations of less than .01 are detectable as statistically significant. The practical effect of correlations this small is not worth being concerned with, in terms of health behaviors, although it is of scientific value. For example, if the r = .01, then 1/10,000th of the total variability in cognitive impairment is accounted for by soy intake (r-squared). I was concerned that the correlation would be high enough that a relatively small sample size could have detected it. Is there anyone who knows the size of the correlation in the large correlational study? R. -----Original Message-----From: numicucamonga [mailto:no-spam-please@...]Sent: Thursday, August 07, 2003 7:44 AM Subject: [ ] Re: Soy Neurotoxicity? Ian wrote: I contacted Lon White, lead researcher in the tofu study to ask some questions. I asked him about the statistical significance of the findings in the study. He informed me that there were four major endpoints in the study:1. cognitive impairment of men (number of men=3734)2. cognitive impairment of sample of wives (n=502)3. brain atrophy by weight of men who died (n=290)4. brain atrophy by volume measured via MRI (n=574) The probability (p) value was less than .05 (significant) for a correlation between each endpoint and tofu intake (there was no significant correlation for other foods).In some cases the p value is less than .001 (if the p value is more than .05, it's not significant, if it's .05 or less, it's significant). Here's what this means:IF p = .05 there's 95% chance the correlation is trueIF p = .01 there's 99% chance the correlation is trueIF p = .001 there's 99.9% chance the correlation is trueSo the correlation between the four endpoints listed aboveand tofu consumption had an over 95% probably of being true,with a probability of truth as high as 99.9%. Of course thiscannot be read as proof that tofu causes those problems, but at the least it signals the need for further investigation.What is perhaps most significant is that Dr White informedme that there is a dose-dependent relationship between tofu consumption and the endpoints, ie, the more tofu was eaten, the more impairment and/or atrophy is found. The odds that such findings would be chance are extremely low! Hi Ian & ALL: What caught my eye is this dose-dependent factor! Since you are an expert on this topic of soy, could you agree that if one ate soy only occasionally, perhaps once per week a glass of soy milk or 1/4 tub of tofu, that one's brain is far less likely to be affected by eating soy? What would be your definition of low risk & time to eat such a quantity of soy noted above? Weekly, bi-weekly, monthly? Going on the idea of moderation, moderation, & dose-dependent there might be a low-risk solution to just eat soy occasionally? Also, since the risk seems related to Genistein are there certain types of soy products you know of that have much less of this substance? Hey, even MR still eats some soy, as it's in one of his recipes, so he must consider occasional soy consumption a risk worth taking too. Your comments & ideas are most welcome. Also, Al Pater, if you read this, what do you think the research shows supporting or contradicting this "danger soy" theory? Thanks! numi .. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2003 Report Share Posted August 7, 2003 This (below) is what I'm wondering about. How come the soy-related dementia only comes out in studies and not among populations that eat lots of soy such as the Okinawans? I don't understand why the writer feels that the study, and not the real-life situation, is more meaningful. S on 8/6/2003 10:53 PM, Ian Goddard at iamgoddard@... wrote: > Evidence Against Soy-Dementia Hypothesis? > > A possible signal contrary to a soy-dementia link is the low > prevalence of dementia [14] and high consumption of soy in Okinawa, > Japan. [15] However, that negative correlation, like any correlation, > does not prove causation. For example, perhaps soy does cause dementia > but other factors in Okinawa offset the effect. > > Also, White et al explored correlations of a range of foods to > neurological parameters, whereas this Okinawa analysis is a sweeping > generalization of only tofu to all of Okinawa. In other words, it > stands to reason that the study by White et al finding a positive > tofu-dementia correlation has the greater likelihood of providing the > more accurate picture. Nevertheless, in my view this Okinawa data > warrants further examination as a possible route to falsifying the > soy-dementia hypotheses. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 7, 2003 Report Share Posted August 7, 2003 " C.B. Rinaldo " <jcrina0@u...> wrote: > Ian, > Thanks VERY much for getting that information from Dr. White. Last night > I was concerned about the findings, but feel better now that I see how large > the sample is. The critical thing for interpreting a finding like this is > the effect size, or the magnitude of the correlation. Luckily, with 3734 > subjects in the study, correlations of less than .01 are detectable as > statistically significant. The practical effect of correlations this small > is not worth being concerned with, in terms of health behaviors, although it > is of scientific value. For example, if the r = .01, then 1/10,000th of > the total variability in cognitive impairment is accounted for by soy intake > (r-squared). I was concerned that the correlation would be high enough that > a relatively small sample size could have detected it. Is there anyone who > knows the size of the correlation in the large correlational study? IAN: Smaller p values mean more significant correlations. No other food reported by the subjects showed any correlation to cognitive impairment and brain atrophy. If you read through this page it's got a lot of matterial that Dr White sent me: http://users.erols.com/igoddard/soy.htm Referring to the section of my post about a negative correlation between soy intake and dementia in Okinawa (where I suggest soy may NOT cause dementia) Francesca asks: " How come the soy-related dementia only comes out in studies and not among populations that eat lots of soy such as the Okinawans? I don't understand why the writer feels that the study, and not the real-life situation, is more meaningful. " But the study by White et al is a real-life study that followed over 3000 people over three decades. I see it as more significant versus the case I presented re Okinawa because it's a peer-reviewed and published study conducted by expert epidemiologists who controlled for a wide range of variables and looked at other foods, whereas my looking at the Okinawa data is just me making a rough " Gee look! " observation. http://IanGoddard.net/cr.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 " numicucamonga " <no-spam-please@a...> wrote: > Hi Ian & ALL: > > What caught my eye is this dose-dependent factor! > > Since you are an expert on this topic of soy, could you > agree that if one ate soy only occasionally, perhaps once > per week a glass of soy milk or 1/4 tub of tofu, that one's > brain is far less likely to be affected by eating soy? IAN: Well, I'd not call myself a soy expert. I do my best to inform myself and cite my sources in whatever I share with others. About the quantities of intake. White el al defined the high-end of tofu consumption as two or more servings per week. In a contemporary health-conscious diet that can be a very LOW intake! Based on that I aim for zero servings per week, but don't worry about it if I eat soy now and then. As the study Al posted shows, higher soy might make you live moderately longer... even if a little dumber. http://IanGoddard.net/journal.htm " To lengthen thy life, lessen thy meals. " Ben lin Ongoing CR-monkey-study update: " In the monkeys...those on reduced feeding since the study started are dying at a rate that is about half that of the monkeys receiving a full food ration. " Associated Press: Eating less may extend human life. August 1, 2002 : http://www.msnbc.com/news/788746.asp?0si=- Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 IAN WROTE: What is perhaps most significant is that Dr White informed me that there is a dose-dependent relationship between tofu consumption and the endpoints, ie, the more tofu was eaten, the more impairment and/or atrophy is found. The odds that such findings would be chance are extremely low! Numi Wrote: What caught my eye is this dose-dependent factor! Since you are an expert on this topic of soy, could you agree that if one ate soy only occasionally, perhaps once per week a glass of soy milk or 1/4 tub of tofu, that one's brain is far less likely to be affected by eating soy? What would be your definition of low risk & time to eat such a quantity of soy noted above? Weekly, bi-weekly, monthly? Going on the idea of moderation, moderation, & dose-dependent there might be a low-risk solution to just eat soy occasionally? IAN WROTE: Well, I'd not call myself a soy expert. I do my best to inform myself and cite my sources in whatever I share with others. About the quantities of intake. White el al defined the high-end of tofu consumption as two or more servings per week. In a contemporary health-conscious diet that can be a very LOW intake! Based on that I aim for zero servings per week, but don't worry about it if I eat soy now and then. As the study Al posted shows, higher soy might make you live moderately longer... even if a little dumber. Hi Ian & ALL: Sorry to refer to you as a " soy expert " . It was interesting to learn you were one heck of a big time eater of soy in times past, so I did not think you would give-up eating soy easily unless convinced otherwise. Referring to your referenced White et al paper & my question about what's a safe amount to eat I decided to look at the full text online here: http://www.jacn.org/cgi/content/full/19/2/242 In table 1 here: http://www.jacn.org/cgi/content/full/19/2/242/T1 It showed in the first 1965 interview only 89 people responded to almost never eating soy vs. 6,218 people responding to eating less than twice per week. Ok, I'm no statistician, but at " face value " how does one draw serious conclusions comparing 89 (data points) people to 6,218 people data points? What's worse is look at the second interview data done in 1971. It shows only 28 people responded (with data) to almost never eating soy vs. 2,547 people responding to eating less than twice per week. Again, I'm no statistician, but at " face value " how does one draw serious scientific conclusions OF MEANING comparing 28 people to 2,547 people? (Meaning, not just playing " the numbers " to derive statistical data, but drawing relevant health conclusions from such sample sizes.) What is the value of such science using such small numbers of people 89 in 1965 & 28 in 1971 who rarely ate soy? Weird science? Valid science? If you know please explain it. Al Pater, do these numbers of test subjects (89 & 28) for one CRITICAL set of data points seem useful -a large enough sample? I believe we need better numbers than this to draw MEANINGFUL conclusions about whether or not to use soy, but someone please explain how my belief is mistaken & this is good science. Thanks sincerely! numi .. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 > Numi Wrote: > > Hi Ian [Goddard] & ALL: > > Sorry to refer to you as a " soy expert " . It was interesting to learn you > were one heck of a big time eater of soy in times past, so I did not think > you would give-up eating soy easily unless convinced otherwise. > > Referring to your referenced White et al paper & my question about what's a > safe amount to eat I decided to look at the full text online here: > > http://www.jacn.org/cgi/content/full/19/2/242 > > In table 1 here: > > http://www.jacn.org/cgi/content/full/19/2/242/T1 > > It showed in the first 1965 interview only 89 people responded to almost > never eating soy vs. 6,218 people responding to eating less than twice per > week. Ok, I'm no statistician, but at " face value " how does one draw > serious conclusions comparing 89 (data points) people to 6,218 people data > points? > > What's worse is look at the second interview data done in 1971. > > It shows only 28 people responded (with data) to almost never eating soy vs. > 2,547 people responding to eating less than twice per week. Again, I'm no > statistician, but at " face value " how does one draw serious scientific > conclusions OF MEANING comparing 28 people to 2,547 people? (Meaning, not > just playing " the numbers " to derive statistical data, but drawing relevant > health conclusions from such sample sizes.) > > What is the value of such science using such small numbers of people 89 in > 1965 & 28 in 1971 who rarely ate soy? Weird science? Valid science? > > If you know please explain it. > > Al Pater, do these numbers of test subjects (89 & 28) for one CRITICAL set > of data points seem useful -a large enough sample? > > I believe we need better numbers than this to draw MEANINGFUL conclusions > about whether or not to use soy, but someone please explain how my belief is > mistaken & this is good science. Hi All, I agree numi. In my opinion, studies in which many are lost in follow-up are highly suspect for confounding, the making the statistical relevance poor. Cheers, Al. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 Hi All, Regarding the numbers of subjects in the study. The sample sizes are sufficient to identify group differences with adequate power, given that the effect sizes are large enough to detect. Here's a useful and (relatively) easy to remember formula for how p-values, effect sizes, and sample sizes relate to one another (which may be of future value): Smaller Probability Values (i.e. higher significance levels) = Effect Size X Size of Study. In other words, to get " significance " one has to have a large-enough-to-detect effect AND adequate sample size. At this point I'll admit, I am a bit of a statistician, or at least, I've taught it at the college level before, and plan to in the future. (My specialty is psychological measurement research, which is one reason I've taken interest in the soy-dementia findings). Regarding the loss of subjects, it sounds like the loss is very serious if this is a longitudinal study. Unfortunately, I've been internet-disabled for almost a week, and haven't been able to get the study itself. If I read the last message right, the sample of 89 original non-soy-eaters dropped to 28? In most cases a 70% loss of subjects in a sample would prevent publication in a top journal, for the reason that Al Pater mentioned. I may have to break down and go to a campus computer to get the article so that I'm not so durn ignorant... R. -----Original Message----- From: old542000 [mailto:apater@...] Sent: Friday, August 08, 2003 6:56 AM Subject: [ ] Re: Soy Neurotoxicity? > Numi Wrote: > > Hi Ian [Goddard] & ALL: > > Sorry to refer to you as a " soy expert " . It was interesting to learn you > were one heck of a big time eater of soy in times past, so I did not think > you would give-up eating soy easily unless convinced otherwise. > > Referring to your referenced White et al paper & my question about what's a > safe amount to eat I decided to look at the full text online here: > > http://www.jacn.org/cgi/content/full/19/2/242 > > In table 1 here: > > http://www.jacn.org/cgi/content/full/19/2/242/T1 > > It showed in the first 1965 interview only 89 people responded to almost > never eating soy vs. 6,218 people responding to eating less than twice per > week. Ok, I'm no statistician, but at " face value " how does one draw > serious conclusions comparing 89 (data points) people to 6,218 people data > points? > > What's worse is look at the second interview data done in 1971. > > It shows only 28 people responded (with data) to almost never eating soy vs. > 2,547 people responding to eating less than twice per week. Again, I'm no > statistician, but at " face value " how does one draw serious scientific > conclusions OF MEANING comparing 28 people to 2,547 people? (Meaning, not > just playing " the numbers " to derive statistical data, but drawing relevant > health conclusions from such sample sizes.) > > What is the value of such science using such small numbers of people 89 in > 1965 & 28 in 1971 who rarely ate soy? Weird science? Valid science? > > If you know please explain it. > > Al Pater, do these numbers of test subjects (89 & 28) for one CRITICAL set > of data points seem useful -a large enough sample? > > I believe we need better numbers than this to draw MEANINGFUL conclusions > about whether or not to use soy, but someone please explain how my belief is > mistaken & this is good science. Hi All, I agree numi. In my opinion, studies in which many are lost in follow-up are highly suspect for confounding, the making the statistical relevance poor. Cheers, Al. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 Wrote: I am a bit of a statistician, or at least, I've taught it at the college level before, and plan to in the future. (My specialty is psychological measurement research, which is one reason I've taken interest in the soy-dementia findings). Hi ! Thanks for taking an interest & posting too. Just a quick related question for you, or Al, or someone else "here" who might know the answer to... I'm certain there are text books on statistics that focus on psychological measurement, but I wonder if such books on statistics are available for nutrition research too? Any thoughts or ideas? Wouldn't it be nice if there was a statistics book for PubMed??? :-) : Regarding the loss of subjects, it sounds like the loss is very serious if this is a longitudinal study. ...If I read the last message right, the sample of 89 original non-soy-eaters dropped to 28? In most cases a 70% loss of subjects in a sample would prevent publication in a top journal, for the reason that Al Pater mentioned. numi: Just to clarify... The lowest (low low) category is *almost* never eating soy (not non-soy-eaters). The 28 that reported data in this lowest category were responders that reported data in '65 & '71 AND were tested for the follow-up cognitive brain function in '91. There were 10 more that were in this category but did not provide data in '71. What's also weird, same lowest group, is 11 of the 28 in '71 reported eating between 1-3 servings of soy the week before, yet these folks were supposed to almost never eat soy? And the next grouping up is for those eating less than 2 servings per week. Also, a large group of '71 non-responders (see where it says no information) in '71 was placed in the low group... low (<twice weekly at the 1965 interview, no information or only one serving in the prior week at the 1971 interview), (That also seems a strange way to stack or place data in one place.) Here is the table that explains more details: http://www.jacn.org/cgi/content-nw/full/19/2/242/F1 Close-up of table: http://www.jacn.org/content/vol19/issue2/images/large/cq0200613001.jpeg More info about above table: At the 1971–1974 examination study participants again received a battery of food frequency questions. At that time they were asked: "During the past week how many servings of tofu did you have?" Responses at this examination were moderately correlated with responses to the tofu intake question asked at the first examination (Pearson r=0.293, p < 0.0001). Fig. 1 presents the conjoint distribution of tofu intake in 1965–1967 and 1971–1974 for all participants whose cognitive function was subsequently evaluated. The number in each cell represents the actual number of men evaluated at the 1991–1993 examination according to their answers to the tofu intake question asked first at the 1965–1967 examination and then again at the 1971–1974 examination. As shown, men in the "low-low" (n=926) and "high-high" (n=271) categories reported consistently low or consistently high tofu intakes at the 1965–1967 and 1971–1974 examinations, while the "low" (n=1574) and "high" (n=962) groups gave less consistent answers, or were classified solely on the basis of their 1965–1967 responses when the 1971–1974 information was missing. Full report here: http://www.jacn.org/cgi/content-nw/full/19/2/242 If you can't see this online let me know, & I'll email it to you as a .pdf file. .. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 8, 2003 Report Share Posted August 8, 2003 Numi's Question: I wonder if such books on statistics are available for nutrition research too? Any thoughts or ideas? Wouldn't it be nice if there was a statistics book for PubMed??? :-) If you live near a university with a medical school, you should be able to find fairly accessible stats texts for the med students in the bookstore. Luckily, stats is not usually a prerequisite for medical school, and most medical programs don't require research productivity, so the med student stats books are usually geared toward helping a person understand and interpret published research. This is my best guess for how to find the most useful book to interpret published research. Oh, don't buy the book there! Just write down the title and order it online, or you may get robbed! Of course, a less effortful way may be to look for course syllabi online for medical school stats classes, and get the textbook titles from them. - Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 9, 2003 Report Share Posted August 9, 2003 " numicucamonga " <no-spam-please@a...> wrote: > > What is the value of such science using such small numbers of people 89 in > 1965 & 28 in 1971 who rarely ate soy? Weird science? Valid science? > > If you know please explain it. IAN: Here's a rebuttle to White et al followed by their responce: http://www.jacn.org/cgi/content/full/19/4/467 As I've noted, laboratory findings are also relevent. The soy phytoestrogen genistein inhibits DNA synthesis in rat cerebral cortex and suppresses a range of neurotrophic (neuroprotective) factor functions. An important example: J Neurochem (Oct 1995): " The ability of the neurotrophic factors to suppress glutamate toxicity and glutamate-induced peroxide accumulation was attenuated by the tyrosine kinase inhibitor genistein, indicating the requirement for tyrosine phosphorylation in the neuro-protective signal transduction mechanism. " http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve & db=PubMed & list_uids=7561872 & dopt=Abstract " Attenuated " of course means " reduced. " Genistein reduced a critical antiaging function. In fact, its well-known that the chemical class to which genistein is a member, tyrosine kinase inhibitors, interfere with neurotrophic (neuroprotective) factors as a class trait. If CR is neuroprotective because it raises neurotrophic factors, the same logic suggests that soy could be neurotoxic for inducing the opposite (even if only in males). In short, the known effects of soy phytochemicals point to a prediction of brain atrophy. In my view, that adds weight to the soy-dementia correlation reported by White et al. http://IanGoddard.net " To lengthen thy life, lessen thy meals. " Ben lin Quote Link to comment Share on other sites More sharing options...
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