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Yogurt FRIES your BRAIN!


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#1 FunkOdyssey

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Posted 23 May 2006 - 07:28 PM


The cultures used to produce yogurt split lactose into glucose and galactose, leaving these two simple sugars as the majority of the sugar content of yogurt. According to recent research, galactose accelerates aging, particularly brain-aging, in mice, rat, and fly models. In some recent studies, galactose is specifically used as an "aging accelerator" to test the protective effects of various supplements against it:

J Neurosci Res. 2006 May 18; [Epub ahead of print]  Related Articles, Links

    Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: Protective effects of R-alpha-lipoic acid.

    Cui X, Zuo P, Zhang Q, Li X, Hu Y, Long J, Packer L, Liu J.

    Institute of Gerontology and Geriatrics, Chinese PLA General Hospital, Beijing, People's Republic of China.

    Chronic systemic exposure of mice, rats, and Drosophila to D-galactose causes the acceleration of senescence and has been used as an aging model. The underlying mechanism is yet unclear. To investigate the mechanisms of neurodegeneration in this model, we studied cognitive function, hippocampal neuronal apoptosis and neurogenesis, and peripheral oxidative stress biomarkers, and also the protective effects of the antioxidant R-alpha-lipoic acid. Chronic systemic exposure of D-galactose (100 mg/kg, s.c., 7 weeks) to mice induced a spatial memory deficit, an increase in cell karyopyknosis, apoptosis and caspase-3 protein levels in hippocampal neurons, a decrease in the number of new neurons in the subgranular zone in the dentate gyrus, a reduction of migration of neural progenitor cells, and an increase in death of newly formed neurons in granular cell layer. The D-galactose exposure also induced an increase in peripheral oxidative stress, including an increase in malondialdehyde, a decrease in total anti-oxidative capabilities (T-AOC), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px) activities. A concomitant treatment with lipoic acid ameliorated cognitive dysfunction and neurodegeneration in the hippocampus, and also reduced peripheral oxidative damage by decreasing malondialdehyde and increasing T-AOC and T-SOD, without an effect on GSH-Px. These findings suggest that chronic D-galactose exposure induces neurodegeneration by enhancing caspase-mediated apoptosis and inhibiting neurogenesis and neuron migration, as well as increasing oxidative damage. In addition, D-galactose-induced toxicity in mice is a useful model for studying the mechanisms of neurodegeneration and neuroprotective drugs and agents. © 2006 Wiley-Liss, Inc.

    PMID: 16710848 [PubMed - as supplied by publisher]

Psychoneuroendocrinology. 2006 May 15; [Epub ahead of print]  Related Articles, Links
    Click here to read
    Effects of d-galactose on the expression of hippocampal peripheral-type benzodiazepine receptor and spatial memory performances in rats.

    Chen CF, Lang SY, Zuo PP, Yang N, Wang XQ, Xia C.

    Department of Neurology, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, China.

    The changes in spatial memory performances and the binding of hippocampal peripheral-type benzodiazepine receptor (PBR) induced by d-galactose (d-gal) were investigated in rats. The animals were randomly divided into two groups: saline-treated group and d-gal-induced aging group. All rats received 56 days of injection followed by 5 days of behavioral tests. The d-gal-induced aging rats presented significant impairment in water maze performance, compared with that in the saline-treated rats. A significant decrease in [(3)H]PK11195 binding in the synaptosomes from hippocampus in the d-gal-induced aging rats was observed, compared to that in the saline-treated rats. Meanwhile, the Scatchard analysis revealed that there was a decrease in B(max), with no significant change in K(D). Further analysis demonstrated that water maze performance was closely related to the PK11195 binding in all rats. These results suggest that d-gal decreased the density of PBR in hippocampal synaptosomes, which may be attributable to the progressive pathogenesis of aging in rats.

    PMID: 16707226 [PubMed - as supplied by publisher]

Behav Brain Res. 2006 May 15; [Epub ahead of print]  Related Articles, Links
    Click here to read
    Quercetin reverses d-galactose induced neurotoxicity in mouse brain.

    Lu J, Zheng YL, Luo L, Wu DM, Sun DX, Feng YJ.

    Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, Xuzhou Normal University, Xuzhou 221116, China; Institute of Molecular Medicine and Genetics Research Center, School of Basic Medical Science, Southeast University, Nanjing 210009, China.

    We assessed the neuroprotective effects of quercetin-feeding at doses of 5 and 10mg/(kgday) on Kunming mice injected daily with d-gal (50mg/(kgday)) by behavioral tests. Quercetin-fed mice showed higher activity upon induction by new environmental stimuli, lower anxiety and higher novelty-seeking behavior in the open field tasks, and significantly improved learning and memory ability in step-through and Morris water Maze tests compared with d-gal-treated mice. We further investigated the mechanisms involved in the neuroprotective effects of quercetin on mouse brain. Quercetin significantly increased superoxide dismutase (SOD) activity and decreased the malondialdehyde (MDA) level. These results imply that quercetin can reverse oxidant impairment induced by d-gal in mouse brain. Neurotoxicity is also associated with Ca(2+) overload induced by oxidant stress. Quercetin could maintain the Ca(2+) homeostasis in the brain of d-gal-treated mice. Furthermore, we also examined the expression of growth-associated protein GAP43 mRNA in mouse brain by in situ hybridization. We found that quercetin dramatically elevated the GAP43 mRNA expression in the brain of d-gal-treated mice to regenerate normal function of neurons against the cellular injury caused by d-gal.

    PMID: 16707173 [PubMed - as supplied by publisher]


WTF is going on here? I've never heard so much as a peep about this before today. Please share your thoughts on the implications of this research and its relevance to humans -- specifically, whether daily ingestion of yogurt could produce negative effects in the brain.

On second thought, any dairy product containing lactose would pose the same problem, because if you are not lactose-intolerant, you will break down the lactose and absorb galactose in the small intestine.

#2 Mind

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Posted 23 May 2006 - 08:25 PM

Please explain the dosing. 100mg/kg? Is that 100mg d-gal per kg of rat? Is this a realistic dosage or is it like the infamous saccharine study that used near lethal amounts to prove a point?

#3 FunkOdyssey

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Posted 23 May 2006 - 08:30 PM

Please explain the dosing. 100mg/kg? Is that 100mg d-gal per kg of rat?

Yes, that's correct. They demonstrated similar effects at 50mg/kg also, which would mean only 3.5g of galactose at 70kg.

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#4 ajnast4r

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Posted 23 May 2006 - 08:31 PM

100 mg/kg = about 8200 grams of d-gal ALONE in an 180lb male. somehow i doubt you will ever ingest that much from yogurt, unless you eat a few galons per day for weeks at a time.

you guys who keep posting these crazy studies really REALLY need to take dosage and situation into account here... + the fact that the health of a caged lab rat being fed feed pelets doesnt = the health of a well fed human... especially not most imminst members whos health is probably many many times greater than average.

#5 FunkOdyssey

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Posted 23 May 2006 - 08:35 PM

100 mg/kg = about 8200 grams of d-gal ALONE in an 180lb male. somehow i doubt you will ever ingest that much from yogurt, unless you eat a few galons per day for weeks at a time.

you guys who keep posting these crazy studies really REALLY need to take dosage and situation into account here... + the fact that the health of a caged lab rat being fed feed pelets doesnt = the health of a well fed human... especially not most imminst members whos health is probably many many times greater than average.

Please check your math -- you might reconsider your position afterward.

There may be some difference in human metabolism of galactose that makes these findings irrelevant to us. I certainly hope so, because I love yogurt.

#6 xanadu

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Posted 23 May 2006 - 08:40 PM

ajnast wrote:

" 100 mg/kg = about 8200 grams of d-gal ALONE in an 180lb male. somehow i doubt you will ever ingest that much from yogurt, unless you eat a few galons per day for weeks at a time."

I think you might want to check your figures, aj. 100mg/kg is one part per 10,000. A 180lb person would be consuming about 8 grams a day

#7 xanadu

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Posted 23 May 2006 - 08:41 PM

Curses! you beat me to it again, Funk. Too slow a typer I guess.

#8 DJS

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Posted 23 May 2006 - 09:06 PM

You're damn right Yogurt will fry your brain!

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#9 Guest_da_sense_*

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Posted 23 May 2006 - 09:14 PM

Well anything on this world has some side effects, if you looked at bad sides of studies we wouldn't even breath air as it oxidizes us :)

Enjoy life, drink your yogurt :)

btw what about probiotic yogurt and kefir yogurt?

#10 ajnast4r

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Posted 23 May 2006 - 09:25 PM

sorry i meant 8200 mg... and what i said still holds

#11 FunkOdyssey

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Posted 23 May 2006 - 09:38 PM

sorry i meant 8200 mg... and what i said still holds

The concern cannot be discounted on account of dosage. You can easily obtain 8g of galactose daily from a diet that includes dairy products. If galactose turns out to be harmless in humans, it will be for another reason. I'm hoping someone with an MR-esque grasp of the science will drop some wisdom on this thread.

#12 ajnast4r

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Posted 24 May 2006 - 01:44 AM

i dont think all of the lactose in non-cultured dairy will be digested by bacteria in the human body... so you cant really count non-cultured dairy.

and i doubt many people consume enough yogurt to achieve 8g galactose... who knows how much lactose is actually split apart in yogurt. obviously not all of it because a lactose intolerant person can not consume yogurt.

thats asuming it even effects are the same on humans. not to mention it was *isolated* and *injected*...not digested along with other co-factors, which can change how certain substances effect the body.

i think its a rediculous concern
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#13 Michael

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Posted 21 June 2006 - 01:52 AM

All:

I'm very sorry not to've gotten back on this until now. I was asked, off-list, to look into this, and I did intend to do some research and get back shortly thereafter, but the research required to come to a satisfactory conclusion seems to be extensive & I'm really very busy on the research and writing front at the moment. Indeed, the possible negative health impacts of the galctose in dairy has been a subject of some concern to me for some years, and I've never fully satisfied myself on the subject.

What first interested me in this issue was the inconsistent but possible epidemiological association between milk consumption and some kinds of cataract, complicated by both , lactose intolerance and unusual galactose metabolism. Looking into the neurodegeneration issue, I can find no meaingful epidemiological evidence; the only study related to the subject is (21), which found a NEGATIVE association of dairy consumption with VASCULAR dementia -- which isn't evidential on neurodegeneratioin per se.

There are five actual or hypothetical issues that I think need explored to evaluate the seriousness of this in general and in any particular person's case:

1. Glycation: galactose glycates proteins much more readily than glucose, so galactose might have a disproportionate effect on AGE.
2. Oxidative stress: galactose appears to cause oxidative stress via reduced GSH levels.
3. Polyol pathway: metabolic conversion of galactose into galactitol in the lens.
4. Riboflavin metabolism: possibly related to (2) or (3). Riboflavin is required for GSH synthesis, and it does seem that
5. Galactosemia: frank galactosemia (overabsorption of galactose -- in humans, at least, this doesn't just flood the system, but has to be actively transported) does undeniably cause cataract. Persons HETEROZYGOUS for the gene polymorphism in question appear to be at higher risk of cataract, & both dairy and riboflavin may be implicated. Unfortunately, such folk are evidently largely asymptomatic, and I have no knowledge that one can get screened, how common heterozygosity is, or whether tracing family history of clinical diseasee would be a reliable way to assess this.

The epidemiology is not totally consistent, but the roles of riboflavin and galactosemia could readily explain inconsistent results in different cohorts.

Fortunately, anyone taking a standard multi should have all the B2 s/he needs (likely an order of magnitude or 2 more, in fact), and many life extension nuts will be taking R(+)-LA and will thus likely have no problems with GSH levels (everyone knows my former and sort-of-ongoing conflict of interest, right? Please don't post this online -- I hate being Googled -- but PM me if you don't know and feel you should).

A bunch of the papers I think relevant, eithe rfrom abstracts or in some cases titles, are appeanded; I would greatly appreciate anyone actively following up to resolve the issue. Anyone taking up the task, please PM me: I have a review on galactosemia that would likely be of help that I'd gladly pass along.

Even if you don't have time to dig in detail, if you're regularly in a bricks-&-mortar university medical library, it'd be great of you to pick up, read, and summarize (19) &/or (19).

Thanks, & apologies for the delay, again.

-Michael

1: Meloni G, Ogana A, Mannazzu MC, Meloni T, Carta F, Carta A. High prevalence of lactose absorbers in patients with presenile cataract from northern Sardinia. Br J Ophthalmol. 1995 Jul;79(7):709. No abstract available. PMID: 7662646 [PubMed - indexed for MEDLINE]

2: Miglior S, Marighi PE, Musicco M, Balestreri C, Nicolosi A, Orzalesi N. Risk factors for cortical, nuclear, posterior subcapsular and mixed cataract: a case-control study. Ophthalmic Epidemiol. 1994 Jun;1(2):93-105. PMID: 8790616 [PubMed - indexed for MEDLINE]

3: Birlouez-Aragon I, Ravelontseheno L, Villate-Cathelineau B, Cathelineau G, Abitbol G. Disturbed galactose metabolism in elderly and diabetic humans is associated with cataract formation. J Nutr. 1993 Aug;123(8):1370-6. PMID: 8336207 [PubMed - indexed for MEDLINE]

4: Arola H, Sillanaukee P, Aine E, Koivula T, Isokoski M. Galactitol is not a cause of senile cataract. Graefes Arch Clin Exp Ophthalmol. 1992;230(3):240-2. PMID: 1597290 [PubMed - indexed for MEDLINE]

5: Couet C, Jan P, Debry G. Lactose and cataract in humans: a review. J Am Coll Nutr. 1991 Feb;10(1):79-86. Review. PMID: 1901325 [PubMed - indexed for MEDLINE]

6: Bhatnagar R, Sharma YR, Vajpayee RB, Madan M, Chhabra VK, Ram N, Mukesh K, Azad RV, Sharma R. Does milk have a cataractogenic effect? Weighing of clinical evidence. Dig Dis Sci. 1989 Nov;34(11):1745-50. PMID: 2582987 [PubMed - indexed for MEDLINE]

7: Sack R, Cohen J. Comparative diets of a idiopathic senile cataract and normal population: dietary risk factors in cataractogenesis. Metab Pediatr Syst Ophthalmol. 1987;10(1):9-13. PMID: 3509278 [PubMed - indexed for MEDLINE]

8: Simonelli F, Savastano S, Rinaldi E, Auricchio G. Cataract formation in diabetic patients and galactose-1-phosphate uridyltransferase deficiency. Ophthalmic Res. 1987;19(5):261-5. PMID: 3438044 [PubMed - indexed for MEDLINE]

9: Hodes BL, Schietroma JM, Lane SS, Sadeghi J, Cunningham D, Stambolian D. Macular deposits in galactokinase deficiency. Metab Pediatr Syst Ophthalmol. 1985;8(2-3):39-42. PMID: 3870945 [PubMed - indexed for MEDLINE]

10: Oski FA. Is bovine milk a health hazard? Pediatrics. 1985 Jan;75(1 Pt 2):182-6. Review. PMID: 3880888 [PubMed - indexed for MEDLINE]

11: Simoons FJ. A geographic approach to senile cataracts: possible links with milk consumption, lactase activity, and galactose metabolism. Dig Dis Sci. 1982 Mar;27(3):257-64. PMID: 6804198 [PubMed - indexed for MEDLINE]

12: Chatterjee A, Milton RC, Thyle S. Prevalence and aetiology of cataract in Punjab. Br J Ophthalmol. 1982 Jan;66(1):35-42. PMID: 7055541 [PubMed - indexed for MEDLINE]

13: Skalka HW, Prchal JT. Presenile cataract formation and decreased activity of galactosemic enzymes. Arch Ophthalmol. 1980 Feb;98(2):269-73. PMID: 7352874 [PubMed - indexed for MEDLINE]

14: Stephens T, Crollini C, Mutton P, Gupta JD, Harley JD. Galactose metabolism in relation to cataract formation in marsupials. Aust J Exp Biol Med Sci. 1975 Jun;53(3):233-9. PMID: 174538 [PubMed - indexed for MEDLINE]

------------ 1: Jacques PF, Taylor A, Moeller S, Hankinson SE, Rogers G, Tung W, Ludovico J, Willett WC, Chylack LT Jr. Long-term nutrient intake and 5-year change in nuclear lens opacities. Arch Ophthalmol. 2005 Apr;123(4):517-26. PMID: 15824226 [PubMed - indexed for MEDLINE]

2: Tarwadi K, Agte V. Linkages of antioxidant, micronutrient, and socioeconomic status with the degree of oxidative stress and lens opacity in indian cataract patients. Nutrition. 2004 Mar;20(3):261-7. PMID: 14990266 [PubMed - indexed for MEDLINE]

3: Sanchez-Castillo CP, Lara J, Romero-Keith J, Castorena G, Villa AR, Lopez N, Pedraza J, Medina O, Rodriguez C, Chavez-Peon Medina F, James WP. Nutrition and cataract in low-income Mexicans: experience in an Eye camp. Arch Latinoam Nutr. 2001 Jun;51(2):113-21. Review. PMID: 11678042 [PubMed - indexed for MEDLINE]

4: Jacques PF, Chylack LT Jr, Hankinson SE, Khu PM, Rogers G, Friend J, Tung W, Wolfe JK, Padhye N, Willett WC, Taylor A. Long-term nutrient intake and early age-related nuclear lens opacities. Arch Ophthalmol. 2001 Jul;119(7):1009-19. PMID: 11448323 [PubMed - indexed for MEDLINE]

5: Cumming RG, Mitchell P, Smith W. Diet and cataract: the Blue Mountains Eye Study. Ophthalmology. 2000 Mar;107(3):450-6. PMID: 10711880 [PubMed - indexed for MEDLINE]

6: Wynn M, Wynn A. Can improved diet contribute to the prevention of cataract? Nutr Health. 1996;11(2):87-104. Review. PMID: 8994232 [PubMed - indexed for MEDLINE]

7: Leske MC, Wu SY, Hyman L, Sperduto R, Underwood B, Chylack LT, Milton RC, Srivastava S, Ansari N. Biochemical factors in the lens opacities. Case-control study. The Lens Opacities Case-Control Study Group. Arch Ophthalmol. 1995 Sep;113(9):1113-9. PMID: 7661743 [PubMed - indexed for MEDLINE]

8: Mares-Perlman JA, Brady WE, Klein BE, Klein R, Haus GJ, Palta M, Ritter LL, Shoff SM. Diet and nuclear lens opacities. Am J Epidemiol. 1995 Feb 15;141(4):322-34. PMID: 7840110 [PubMed - indexed for MEDLINE]

9: Sperduto RD, Hu TS, Milton RC, Zhao JL, Everett DF, Cheng QF, Blot WJ, Bing L, Taylor PR, Li JY, et al. The Linxian cataract studies. Two nutrition intervention trials. Arch Ophthalmol. 1993 Sep;111(9):1246-53. PMID: 8363468 [PubMed - indexed for MEDLINE]

10: Hankinson SE, Stampfer MJ, Seddon JM, Colditz GA, Rosner B, Speizer FE, Willett WC. Nutrient intake and cataract extraction in women: a prospective study. BMJ. 1992 Aug 8;305(6849):335-9. PMID: 1392884 [PubMed - indexed for MEDLINE]

11: Straatsma BR, Lightfoot DO, Barke RM, Horwitz J. Lens capsule and epithelium in age-related cataract. Am J Ophthalmol. 1991 Sep 15;112(3):283-96. PMID: 1882940 [PubMed - indexed for MEDLINE]

12: Leske MC, Chylack LT Jr, Wu SY. The Lens Opacities Case-Control Study. Risk factors for cataract. Arch Ophthalmol. 1991 Feb;109(2):244-51. PMID: 1993036 [PubMed - indexed for MEDLINE]

13: Bunce GE, Kinoshita J, Horwitz J. Nutritional factors in cataract. Annu Rev Nutr. 1990;10:233-54. Review. PMID: 2200464 [PubMed - indexed for MEDLINE]

14: Jacques PF, Hartz SC, Chylack LT Jr, McGandy RB, Sadowski JA. Nutritional status in persons with and without senile cataract: blood vitamin and mineral levels. Am J Clin Nutr. 1988 Jul;48(1):152-8. PMID: 3389322 [PubMed - indexed for MEDLINE]

15: Sack R, Cohen J. Comparative diets of a idiopathic senile cataract and normal population: dietary risk factors in cataractogenesis. Metab Pediatr Syst Ophthalmol. 1987;10(1):9-13. PMID: 3509278 [PubMed - indexed for MEDLINE]

16: Skalka HW, Prchal JT. Cataracts and riboflavin deficiency. Am J Clin Nutr. 1981 May;34(5):861-3. PMID: 7234715 [PubMed - indexed for MEDLINE]

17: Prchal JT, Conrad ME, Skalka HW. Association of presenile cataracts with heterozygosity for galactosaemic states and with riboflavin deficiency. Lancet. 1978 Jan 7;1(8054):12-3. PMID: 74495 [PubMed - indexed for MEDLINE]

18: [No authors listed] Riboflavin deficiency, galactose metabolism and cataract. Nutr Rev. 1976 Mar;34(3):77-9. Review. No abstract available. PMID: 176612 [PubMed - indexed for MEDLINE]

19: Seetharam Bhat K, Gopalan C. Human cataract and galactose metabolism. Nutr Metab. 1974;17(1):1-8. No abstract available. PMID: 4370075 [PubMed - indexed for MEDLINE]

20: Srivastava SK, Beutler E. Increased susceptibility of riboflavin deficient rats to galactose cataract. Experientia. 1970 Mar 15;26(3):250. No abstract available. PMID: 5417478 [PubMed - indexed for MEDLINE]

21. Yamada M, Kasagi F, Sasaki H, Masunari N, Mimori Y, Suzuki G. Association between dementia and midlife risk factors: the Radiation Effects Research Foundation Adult Health Study. J Am Geriatr Soc. 2003 Mar;51(3):410-4. PMID: 12588587 [PubMed - indexed for MEDLINE]
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#14 John Schloendorn

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Posted 21 June 2006 - 02:45 AM

You're damn right Yogurt will fry your brain!

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#15 FunkOdyssey

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Posted 21 June 2006 - 03:45 AM

I'm very sorry not to've gotten back on this until now. I was asked, off-list, to look into this, and I did intend to do some research and get back shortly thereafter, but the research required to come to a satisfactory conclusion seems to be extensive & I'm really very busy on the research and writing front at the moment. Indeed, the possible negative health impacts of the galctose in dairy has been a subject of some concern to me for some years, and I've never fully satisfied myself on the subject.

Thanks for getting back to me on this, and no worries about the delay. [thumb]

#16 Infernity

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Posted 21 June 2006 - 09:07 PM

Yogurt helps the immune system... Everything has advantages and disadvantages, you must find the balance.

You have researches for all sides, it all depends on who funds it.


-Infernity

#17 Sillewater

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Posted 25 June 2010 - 06:09 AM

In this review (I haven't read the whole thing) it says that yoghurt wasn't a problem, since this study I haven't found anything else on the subject:

J Nutr. 1993 Aug;123(8):1370-6.

Disturbed galactose metabolism in elderly and diabetic humans is associated with cataract formation.
Birlouez-Aragon I, Ravelontseheno L, Villate-Cathelineau B, Cathelineau G, Abitbol G.

Analytical Chemistry Laboratory, Institut National Agronomique, Paris, France.

..We conclude that the cataractogenic action of milk lactose is dependent on the disturbance of galactose metabolism in elderly subjects and that yogurt is not cataractogenic, although the mechanism of the protective effect of yogurt remains unknown



In the paper they state that non-diabetics drinking >100ml or >200ml had a relative risk of 2.7 and 4.0 respectively (P<0.05).
It definitely does seem like as we get older the amount of galactose floating in our blood gets higher (from the amount we ingested).

Based on this study:

Metabolism. 2009 Aug;58(8):1050-8. Epub 2009 Jun 18.

Contribution of galactose and fructose to glucose homeostasis.
Coss-Bu JA, Sunehag AL, Haymond MW.

Department of Pediatrics, Children's Nutrition Research Center, US Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston, TX 77030, USA.



a drink bolus of "(0.72 g/kg) of galactose labeled to 2% with [U-13C]galactose (protocol A)" resulted in:


Plasma galactose concentrations
The plasma galactose concentrations were 0.07 ± 0.01, 2.57 ± 0.53, 0.73 ± 0.26, 0.16 ± 0.04, 0.10 ± 0.03, and 0.07 ± 0.01 mmol/L at 0, 1, 2, 3, 4, and 5 hours, respectively, in protocol A.



which doesn't seem very high. Considering on average the subjects consumed 50g of galactose.
But the epidemiological evidence definitely shows a relationship between lactose consumption and various diseases:

Nutr Cancer. 2008;60(3):292-300.

Impact of lactose containing foods and the genetics of lactase on diseases: an analytical review of population data.
Shrier I, Szilagyi A, Correa JA.

Centre for Clinical Epidemiology and Community Studies, Sir Mortimer B Davis Jewish General Hospital, McGill University, Montreal, Quebec, Canada.

Abstract
Dairy foods (DFs) contain complex ingredients that could affect different diseases. The control of lactose digestion phenotypically divides populations into those who can [lactase persistent (LP)] and those who cannot [lactase nonpersistent (LNP)] assimilate lactose. LNP subjects, however, can adapt to lactose intolerance through intestinal bacteria. The DF/LNP status interactions may function as disease risk modifiers. We evaluated the relationship between DF and LNP with colorectal, breast, prostate, ovarian, lung, and stomach cancer and inflammatory bowel diseases (IBD; Crohn's disease and ulcerative colitis). Yearly per capita DF consumption, LNP national prevalence, cancer mortality, and incidence of IBD were obtained from several sources. A negative binomial regression model was used to derive incremental risks. There were statistically significant (P <or= 0.05) increases in risk for colorectal and prostate cancer and ulcerative colitis with DFs and a statistically significant decreased risk for stomach cancer. There were trends (P<0.1) for lung and ovarian cancers and Crohn's disease. As LNP prevalence increased, stomach cancer risk increased, whereas risks of all other conditions decreased (P<0.01). In 3 cancers (prostate, ovarian, and breast), meta-analyses of case-based studies support ecological data. In colorectal cancer, on the contrary, meta-analyses of case-based studies suggest protection. The possible importance of distinguishing LNP/LP status in studies is discussed.

PMID: 18444163 [PubMed - indexed for MEDLINE]



this is a very good review on brain damage due to metabolic disorders:

Brain Damage in Phenylalanine, Homocysteine and Galactose Metabolic Disorders

Apparently its the white matter that is damaged (maybe all dairy-eaters should take some methylcobalamin).

Here's a fairly recent review of the galactose issue:

IUBMB Life. 2009 Nov;61(11):1063-74.

Galactose toxicity in animals.
Lai K, Elsas LJ, Wierenga KJ.

Division of Medical Genetics, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. kent.lai@hsc.utah.edu


Abstract
In most organisms, productive utilization of galactose requires the highly conserved Leloir pathway of galactose metabolism. Yet, if this metabolic pathway is perturbed due to congenital deficiencies of the three associated enzymes, or an overwhelming presence of galactose, this monosaccharide which is abundantly present in milk and many non-dairy foodstuffs, will become highly toxic to humans and animals. Despite more than four decades of intense research, little is known about the molecular mechanisms of galactose toxicity in human patients and animal models. In this contemporary review, we take a unique approach to present an overview of galactose toxicity resulting from the three known congenital disorders of galactose metabolism and from experimental hypergalactosemia. Additionally, we update the reader about research progress on animal models, as well as advances in clinical management and therapies of these disorders.

PMID: 19859980 [PubMed - indexed for MEDLINE]PMCID: PMC2788023 [Available on 2010/11/1]




In the review they mention:


<a name="SEC2-4" style="color: rgb(51, 102, 153); text-decoration: none; ">Perturbation of Inositol MetabolismWells and Wells reported decreased free and lipid-bound inositol in the tissues of both GALT-deficient patients ([116]) and galactose-intoxicated rats ([117]). Recently, over-expression of human inositol monophosphatase was found to overcome galactose toxicity in GALT-deficient yeast cells ([95]). Furthermore, gal-1-P competitively inhibited human inositol monophosphatase ([118]). These recent findings suggest a pathogenic role of reduced inositol pools in GALT-deficiency.

These proposed mechanisms for gal-1-P toxicity are not mutually exclusive. For instance, it is possible that the loss of sialic acids in some of the glycoproteins detected under GALT-deficiency resulted from both UDP-galactose deficiency ([107][119]) and from excess galactitol formation ([120]). Similarly, myo-inositol deficiency could be due to both excess galactitol accumulation ([30]) and inhibition of inositol phosphatases by excess gal-1-P ([118]).



Sorry for the long post. Anyways, for now I'm ditching the milk. Have to find to get calcium somewhere else.

Edited by Sillewater, 25 June 2010 - 06:13 AM.


#18 Sillewater

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Posted 25 June 2010 - 06:19 AM

There also seems to be a lot of studies done in the past on aldose reductase inhibitors and galactose induced cataracts:



Arch Ophthalmol. 1990 Sep;108(9):1301-9.


Prevention of retinal vessel changes associated with diabetic retinopathy in galactose-fed dogs by aldose reductase inhibitors.
Kador PF, Akagi Y, Takahashi Y, Ikebe H, Wyman M, Kinoshita JH.

National Eye Institute, National Institutes of Health, Bethesda, Md 20892.


Abstract
Vascular changes associated with early diabetic retinopathy that include the selective degeneration of pericytes, the formation of microaneurysms and acellular capillaries, and vessel dilation have been experimentally investigated in age- and sex-matched beagle dogs fed a 30% galactose diet and treated with or without the aldose reductase inhibitors sorbinil and/or M79175. Eyes from dogs in each group were periodically enucleated during a 36-month period and their retinal capillaries were examined as trypsin-digested flat preparations. These studies reveal that the destruction of retinal pericytes to form pericyte ghosts is the earliest observable retinal vessel change occurring after 19 to 21 months of galactose feeding. By 24 months, both an irregular distribution of endothelial cell nuclei near pericyte ghosts and the presence of acellular capillaries containing neither endothelial cells nor pericytes can be observed. This was followed by the histologic appearance of microaneurysms after 27 months and the funduscopic appearance of intraretinal hemorrhages after 33 months. Varicose enlargements of capillaries were also observed in the trypsin-digested preparations from dogs fed galactose for 33 to 36 months. All of these changes are linked to the initial aldose reductase-associated destruction of pericytes. The onset and progression of these retinal changes were retarded in a dose-dependent manner with aldose reductase inhibitors.

PMID: 2119169 [PubMed - indexed for MEDLINE]



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#19 Soma

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Posted 14 July 2010 - 06:10 PM

Isn't yogurt something that is consumed rather regularly in the Mediterranean regions?

From the Mayo Clinic:
Posted Image
http://www.mayoclini...an-diet/CL00011

You can drive yourself absolutely crazy trying to deconstruct blatantly contradictory study results.

#20 Logan

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Posted 14 July 2010 - 06:37 PM

As far as I'm concerned, if you are getting proper regular exercise, avoiding stress, eating right, and avoiding excess sugar, you shouldn't have to worry about consuming a little yogurt everyday. At least I hope not, I drink Kefir and eat yogurt everyday.

#21 Soma

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Posted 15 July 2010 - 03:16 AM

As far as I'm concerned, if you are getting proper regular exercise, avoiding stress, eating right, and avoiding excess sugar, you shouldn't have to worry about consuming a little yogurt everyday. At least I hope not, I drink Kefir and eat yogurt everyday.


Well, that's just the thing.

Proper regular exercise, avoiding stress, and avoiding excess sugar are all relatively straight forward, in terms of accomplishing such ideals.

"Eating right" on the other hand, is not even close to being clear cut. There are innumerable theories posited by researchers and nutritionists circulating as to what constitutes the "right" way of eating. For every one of those theories, there are countervailing theories.

The entire concept of "eating right" is entirely ambiguous, and the practice of such is relative.

Don't get me wrong- I obviously understand your main thrust. But there's an endless sea of seemingly viable opinions and viewpoints and each of them, to one extent or another, tend to have some degree or form of validity.

#22 niner

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Posted 15 July 2010 - 04:20 AM

The questions here are how much galactose is in yogurt, and what does the dose/harm relationship look like? It looks like a really huge amount of galactose in your diet is bad. But small amounts? Maybe not so bad. Lai et al. (above) say:

In most organisms, productive utilization of galactose requires the highly conserved Leloir pathway of galactose metabolism. Yet, if this metabolic pathway is perturbed due to congenital deficiencies of the three associated enzymes, or an overwhelming presence of galactose, this monosaccharide which is abundantly present in milk and many non-dairy foodstuffs, will become highly toxic to humans and animals.

I read this as saying that as long as you have normal galactose metabolism and you don't overdose on galactose, you should be ok. My dairy consumption is already on the low side. I don't plan to drop it, but in view of some of the epidemiology, I don't think I'll make any effort to increase it either.

#23 e Volution

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Posted 15 July 2010 - 04:51 AM

^^ Well said niner, this is my thoughts exactly. It certainly feels like none > some but we are trying to find a diet/eating regimen for life and this has it's own set of requirements of being varied, satisfying, and convenient and a host of other factors that play into it. I noticed when I first went Paleo I was too strict, and I ended up 'cheating' and binging quite excessively from time to time usually on the weekends. I am now of the opinion that including a few [possibly] less than ideal foods like yoghurt and some cheese or consuming a bit more of what may be optimal of dark chocolate for example; is much better than not being completely satisfied with your food and as a result being exposed to the real bad stuff like trans-fats, oxidised n-6, HFCS, preservatives/chemicals, (and for us Paleo folks gluten-grains), etc.

#24 timar

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Posted 27 March 2015 - 08:57 AM

I just came across this silly titled topic and, well...

 

double-facepalm.png

 

 

A good example of how an incomplete and reductionist understanding of a certain subject can lead to completely pointless concerns...

 

Seriously, guys, has it occured to noone here, that unless you suffer from lactose intolerance, the enzymes in your gut do exactly the same job the bacteria in the yogurt do - to cleave the lactose disaccharide bonds - and that it doesn't matter at all whether you ingest the galactose as a monosaccharide or in the form of lactose, just as it doesn't matter whether you ingest fructose as monosaccharide or as plain sugar (saccharose)?

 

However, during fermentation the bacteria consume some of the galactose, hence fermented milk products actually contain lower levels of digestible galactose than non-fermented milk. Interestingly, the few epidemiological studies discerning milk from fermented dairy have shown beneficial effects from the latter but not from the former. A recent Swedish cohort study found that high milk consumption was associated with a marked increase in all-cause mortality (almost twofold for two glasses a day), whereas fermented dairy (yogurt and cheese) actually seem to have the opposite effect - a statistically significant decrease in all-cause mortality (although somewhat varying over intake levels, the data is burried in the appendix, btw.).

 

The authors' conclusion is that the reduced galactose content due to fermentation may be responsible for the observed opposite effects. This may be true for cheese, which usually contains only trace amounts of lactose and galactose, but does not explain the magnitude of difference in the outcomes with regard to yogurt, as the galactose content of yogurt is reduced only by about 20-30% by fermentation and in low- and non-fat yogurt the lactose content is usually even higher than in milk because additional milk powder is added to improve taste and texture. My take is that we should not once again step in the reductionist trap here and reduce the health effects of a complex food to one of its main compounds. It may be that reduced galactose levels contributes to the health benefits of yogurt over milk, but there have to be some additional beneficial compounds derived from fermentation being responsible for the difference.

 

Here's a recent video from Michael Greger discussing the Swedish study (Of course given his vegan agenda, he stresses the dangers of galactose from milk and quickly skips over the observed benefits for fermented dairy - but at least he did manage to mention it at all):

 


Edited by timar, 27 March 2015 - 08:59 AM.


#25 zorba990

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Posted 27 March 2015 - 11:17 PM

Human breastmilk contains lots of lactose
https://m.facebook.c...503726189655655
The above study might not be applicable to humans unless they have galactosemia

http://m.ilarjournal...nt/43/2/66.full

Edited by zorba990, 27 March 2015 - 11:23 PM.


#26 Babol

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Posted 04 April 2015 - 11:06 AM

Really? Yougurt? I thought it is healthy)))



#27 BigLabRat

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Posted 03 June 2015 - 11:24 PM

If you're really concerned about the residual sugars in yogurt, strain it before you eat it. The galactose, glucose, and remaining lactose are all concentrated in the whey rather than the protein/fat complexes. Cheesecloth and a colander will do.

 

It should be noted that many of the cultures that consume large amounts of yogurt (Greek, Arab, Indian) do so in a highly strained form, all the way from 'Greek-style' yogurt to labneh to yogurt cheeses.

 

The whey itself is odd stuff--sort of glowing chartreuse because of the riboflavin. (It shouldn't be confused with whey from cheese, which is full of proteins; yogurt whey is acidic and contains mostly sugars and some vitamins.)

 

How much sugar remains in the yogurt, of course, depends on how long you strain it, but I've heard that if you reduce it to a Greek consistency it takes out about half the sugars, and if you go all the way to heavy cream cheese, you have removed perhaps 70%.

 

In any case, you have far less sugars than were in the milk to begin with!  



#28 Groundhog Day

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Posted 03 October 2015 - 02:41 PM

This topic is very interesting to me....I've been lactose intolerant for the last 16-17 years but have always been able to easily digest yogurt. In fact, I suffer from chronic severe insomnia, and found a correlation with yogurt consumption and the ability to sleep at all in the last few years. I narrowed it down to L.Rhamnosus as the specific strain in yogurt...looking at studies the mechanism is likely lowered histamine or immune system modulation/regulation...it also lowers anxiety.

 

The problem I have is that I also have some signs of neurodegeneration and the requirement for yogurt to have a chance to sleep has actually gone up to about 1 cup a day, maybe a little more. I'm trying to find other sources of L.Rhamnosus, such as probiotic supplements, but so far none of them have worked. There must be other co-factors or the overall absorption is much higher with sugar.

 

Am I interpreting this correctly? That lactose intolerant people will automatically handle galactose improperly?



#29 NeuroNootropic

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Posted 02 January 2016 - 04:40 AM

So what's the consensus on this? Is milk good or bad?



#30 Groundhog Day

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Posted 02 January 2016 - 03:50 PM

I think the verdict is in on milk...it's bad, but the case with yogurt is a little more cloudy... there is still significant galactose content in most yogurts.






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