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Sibiriak: 2) A curcumin supplement designed for enhanced bioavailability,  such as Longvida or Meriva, which are quite different from each other.    That's a topic in itself.


Btw, there are quite a few scientific papers on curcumin(oid) bioavailabilty, but another very interesting source of info is the patent applications for various curcumin formulas.


I just read through the Longvida Patent application (by The Regents of the University of California),  and it's a treasure trove of interesting facts and ideas.  Some of them I already knew to some extent, but others are real hidden gems.


Bioavailable curcuminoid formulations for treating alzheimer's disease and other age-related disorders

EP 1993365 B1

For example:

Formula 1. PC-DHA curcumin/tetrahydrocurcumin micelles

  • [0046] Curcumin, tetrahydrocurcumin (enhances absorption, synergizes with curcumin), phosphatidylcholine (emulsifies, makes micelles with deoxycholate salt, greatly enhances absorption), docosahexaenoic acid (from marine oil; synergizes with curcumin, facilitates curcumin delivery to brain or tumors), an antioxidant or antioxidant mix (vitamin C or lipodated vitamin C, alpha-lipoic acid, vitamin E) (used to stabilize and recycle curcumin, maintaining its stability and preventing it from becoming a pro-oxidant in the capsule or in the body).


Formula 2. PC-DHA curcumin micelle

  • [0047] Curcumin (we have determined that 25% of curcuminoids in plasma are naturally converted to tetrahydrocurcumin which enhances absorption, synergizes with curcumin), phosphatidylcholine, docosahexaenoic acid, an antioxidant or antioxidant mix (vitamin C or lipodated vitamin C, alpha-lipoic acid, vitamin E)


Formula 3. Olive oil/DHA curcumin

  • [0048] Curcumin, docosahexaenoic acid, an antioxidant or antioxidant mix (vitamin C or lipodated vitamin C, alpha lipoic acid, vitamin E). Our data shows that when curcumin is dissolved in oil, plasma curcumin remains low, but red blood cell curcumin is quite high, which explains bioavailability despite negligible plasma levels. No other group has reported this fundamental observation that appears to be the simplest method of enhancing bioavailability. Other healthful oils can be used (fish oil, canola oil, other high omega-3 oil). In this formulation, curcumin in oil can be microencapsulated.


This topic is too complex for this thread--I only point out this source  to those rare birds who might be looking  into it deeply.

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Thanks Sibiriak, turmeric powdered or cooked, together with EVOO (and black pepper) appears to  be a very good natural combo, according to the info you posted. I always use EVOO together with turmeric since I just throw it liberally into the plates. Piperine in the presence of oils should be redundant but redundant safety systems work notoriously better...

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Mccoy,  if I understand correctly, the oil and piperine  are not really redundant since the oil increases GI absorption (solubilization) while the piperine inhibits glucuronidation in the liver.


From the patent application linked above:


Three factors limit curcumin absorption and need to be addressed: 1) rapid glucuronidation/sulfation of curcumin's phenolic hydroxyl groups and high "first pass" clearance; 2) curcumin is unstable in aqueous solution at pH 7 and above; and 3) curcumin is very hydrophobic and typically is not water soluble at acidic pH and when delivered as a dry powder in existing supplements. (Most of the curcumin is never absorbed and simply passes through the GI tract and is excreted.)


There are, however, arguments against inhibition of glucuronidation via piperine or other agents:


The major U.S. supplier, Sabinsa, has tried to make a more bioavailable form by adding Bioperine (piperine) to inhibit glucuronidation. Such an approach is flawed, however, because most glucuronidation takes place in the upper GI tract, where the pH is acidic, and curcumin is not completely dissolved until pH 8.5 and higher. Even worse, inhibiting glucuronidation can cause serious health risks. Glucuronidation is protective against many toxins and involved in the metabolism of commonly used drugs. Most elderly patients are on multiple drugs, at levels likely to be unsafely altered by inhibition of glucuronidation.


Of course, this may not be an issue if you are not taking any medications--still, there may be other toxins you want to be protected against, and continuous long-term piperine use may degrade that protection.  Or so it is argued. The dangers are probably exaggerated.  Also: studies on curcumin w/ piperine show a very quick spike in curcumin plasma levels, and some writers have questioned the real value of that effect. (I'd have to dig up the info on that to be more precise.   There are  also some interesting issues regarding the bioactivity of curcumin metabolites.) 


The Longvida curcumin formula does not use piperine, but does include some water-soluble antioxidant.


To protect the curcuminoid against hydrolysis, a water-soluble antioxidant is employed. Nonlimiting examples include ascorbic acid (ascorbate, vitamin C and its acylated fat soluble derivatives), α-lipoic acid (alpha-lipoate), vitamin E and derivatives, N-acetylcysteine (NAC), and reduced glutathione (GSH). Even tetrahydrocurcumin provides curcumin some protection against hydrolysis. Mixtures of antioxidants also can be used.


We have tested serial dilutions of ascorbate and find stabilization is effective out to 4 hours (a typical absorption cycle), with curcumin:ascorbate ratios as high as 16: 1, with some small decline in efficacy between 8:1 and 16:1. Therefore, providing a curcuminoid-to-antioxidant ratio of about 10:1 or higher should be sufficient to prevent hydrolysis during absorption, and enhance bioavailability. As one nonlimiting example, a preparation containing 330 mg of curcumin (MW 368) would have only an additional 17.75 mg of ascorbate (MW 198).


And it includes DHA for the reasons quoted in my previous post.   (Longvida curcumin was designed for  brain-protection primarily. ) I found it quite interesting that "when curcumin is dissolved in oil, plasma curcumin remains low, but red blood cell curcumin is quite high."     Practically every study I've read deals only with plasma levels.  


Using turmeric with oil is an age-old practice.  There is a lot of info from a less scientific point of view at  the "Turmeric for Health" web site.  One commenter  from India  suggested another way to consume turmeric:


Kumar (India)

February 21, 2016 at 10:54 pm

The best way to consume turmeric is to mix its powder in oats along with identical quantity of black pepper powder, boil the mixture in water for a few minutes and consume it in the morning. The ideal dosage is three tablespoon full of oats, one third teaspoon of turmeric powder and one third teaspoon of black pepper powder. Oats acts as a vehicle to deliver turmeric powder and pepper powder, apart from being a rich source of fibre. This mixture also acts as a preventive measure for many ailments/diseases like common cold/flu/cough/body pains/arthritis,etc.This has been tested and proven 100 per cent and I am fully convinced and satisfied with the wonderful results.


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Mccoy: It's unfortunate that the pharmacokinetics of curcumin still seems to be not perfectly understood.


Yes, it's all extremely complex, and there will not be any complete answers for a  long time.  A glance at this article will give you an idea of how complex some of the issues are:





PMCID: PMC4335222


Curcumin autoxidizes at physiological pH to a spectrum of dioxygenated metabolites with electrophilic, as well as nucleophilic moieties. The previously unrecognized diversity of chemical entities formed in the autoxidation (quinone methide, peroxyl radical, endoperoxide, spiroepoxide, vinylether, cyclopentadione, etc.) is remarkable. Undoubtedly, this provides a novel paradigm to understand the vast cellular effects of curcumin (polypharmacology) based on the number and diversity of its spontaneous transformation products.


These new insights are pointing toward much greater bioactivity of curcumin metabolites than previously suspected.
Oxidative metabolism of curcumin-glucuronide by peroxidases and isolated human leukocytes.




Conjugation with glucuronic acid is a prevalent metabolic pathway of orally administrated curcumin, the bioactive diphenol of the spice turmeric. The major in vitro degradation reaction of curcumin is autoxidative transformation resulting in oxygenation and cyclization of the heptadienedione chain to form cyclopentadione derivatives. Here we show that curcumin-glucuronide is much more stable than curcumin, degrading about two orders of magnitude slower. Horseradish peroxidase-catalyzed oxidation of curcumin-glucuronide occurred at about 80% of the rate with curcumin, achieving efficient transformation. Using LC-MS and NMR analyses the major products of oxidative transformation were identified as glucuronidated bicyclopentadione diastereomers. Cleavage into vanillin-glucuronide accounted for about 10% of the products. Myeloperoxidase and lactoperoxidase oxidized curcumin-glucuronide whereas tyrosinase and xanthine oxidase were not active. Phorbol ester-activated primary human leukocytes showed increased oxidative transformation of curcumin-glucuronide which was inhibited by the peroxidase inhibitor sodium azide.


These studies provide evidence that the glucuronide of curcumin is not an inert product and may undergo further enzymatic and non-enzymatic metabolism. Oxidative transformation by leukocyte myeloperoxidase may represent a novel metabolic pathway of curcumin and its glucuronide conjugate.


Interestingly, a 2015 study on diabetic rats pointed to the importance of curcumin metabolites and found that piperine could nullify the positive curcumin effects.


Curcumin Pharmacokinetic and Pharmacodynamic Evidences in Streptozotocin-Diabetic Rats Support the Antidiabetic Activity to Be via Metabolite(s)




Our results showed that one single administration of curcumin was not sufficient to improve the ability of STZ-diabetic rats to reverse hyperglycemia. However, in the 1st day of curcumin treatment, it is interesting to note that these rats showed a fast decrease in the glycemia after 105 and 120 minutes of the glucose overload, when compared with untreated-diabetic rats (Figure 3(a)).


This finding reiterates the pharmacokinetic data on the possibility of the beneficial effects of curcumin to be exerting by a metabolite(s), which need an additional time to reach the therapeutic levels and to control the glucose metabolism. In fact, it was observed that the treatment for 15 days with curcumin promoted a most evident benefit on glucose metabolism of diabetic rats, improving both the glucose tolerance (Figure 3©) and the insulin sensitivity (Figure 4© and inserted table).


Long-term of a daily treatment with curcumin probably culminates in an increased permanence into the circulation of the curcumin metabolite(s), allowing the biological active compound(s) to exert its effects in a most pronounced way. Recent evidence of our laboratory reinforces the possibility of the antidiabetic activity of curcumin to be exerted by metabolite(s): Arcaro et al. [15] found that the treatment of STZ-diabetic rats with yoghurt enriched with 90 mg/kg curcumin and piperine did not increase (20 mg/kg piperine) and even nullified (40 mg/kg piperine) the antidiabetic and antioxidant activities of curcumin. It is well known that piperine increases the bioavailability of many drugs and compounds, including curcumin, via inhibition of the activity of various metabolizing enzymes found in liver and intestine, such as aryl hydroxylases, N-demethylases, UDP-glucuronyltransferases, and cytochrome P450 3A4 [39, 40]. However, the inhibition of the curcumin biotransformation will not necessarily lead to an increase of its pharmacodynamic actions, and indeed adverse effects can be reached.


Corroborating the hypothesis that curcumin metabolite(s) has pivotal importance in determined biological activities when curcumin is administered orally, Neyrinck et al. [41] found that the coadministration of curcuma extract (0.1% of curcumin) and 0.01% of white pepper (which contains piperine) to mice fed a high-fat (HF) diet did not promote any change in the glucose and lipid homeostasis, in comparison with nontreated HF mice. Besides, HF mice receiving these phytotherapics showed low levels of proinflammatory cytokines IL-6 and TNF-α in subcutaneous adipose tissue in association with accumulation of THC; the authors suggested that this metabolite may be responsible for the anti-inflammatory response.

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Mccoy,  perhaps you could help me satisfy my curiosity.


An Italian scientist, Dr. Francesco Di Pierro,  has a patent/application  for a  curcumin formulation containing a phospholipid-curcumin complex and piperine.




[An Italian company, Indena, has the patent for the curcumin phospholipid complex (aka "phytosome") which goes by the name Meriva.  For info on phytosomes,  see "Phytosome and Liposome: The Beneficial Encapsulation Systems in Drug Delivery and Food Application"

http://journals.sbmu.ac.ir/afb/article/download/8832/pdf_23 ]


Dr. Di Pierro conducted a study on neuropathic pain patients using a curcumin phytosome/piperine/lipoic acid  combination that is marketed in Italy as "Lipicur".




He has a short video on YouTube titled "Dr.Francesco Di Pierro - Fitoterapici in Oncologia " in which he discussed his curcumin formulation, the above mentioned study, and curcumin in relation to cancer.



I'm curious what you think of him.   All I know is I love the way he pronounces "piperina" in Italian. :Dxyz   

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Rhonda Patrick interviews Jed Fahey,  preeminent expert on isothiocyanates, sulforaphane,  broccoli extracts etc. It's long, but covers a lot of  interesting  topics. 





Jed Fahey, Sc.D. on Isothiocyanates, the Nrf2 Pathway, Moringa & Sulforaphane Supplementation

Dr. Jed Fahey is a multi-decade veteran of isothiocyanate research and is the director of the Cullman Chemoprotection Center at Johns Hopkins University. Much of this conversation, as you might expect given Dr. Fahey's pedigree as a research scientist, is focused on isothiocyanates and, indeed, sulforaphane!  While we covered quite a lot on this very topic (isothiocyanates) via my solo podcast a few weeks ago, this covers everything that may have been overlooked.... and, indeed, so much more! Skip to the timeline below for a sampling.  Dr. Fahey and his colleagues have been, in a big way, at the absolute center of what is a staggering amount of research on these very powerful compounds. There is hardly a topic which we can discuss in which he doesn't have an anecdote about a study he was involved in, or, in some cases, tribal knowledge that may not even be published but is nonetheless interesting and an important part of the story that is unique to his particular vantage point.  In this 2-hour and 30-minute interview, we discuss...  [times may not be accurate]

  • 00:00:00 - the early history of sulforaphane research, including key initial discoveries.
  • 00:00:37 - the serendipitous unfolding of events that lead to the converging of the research on the NRF2 stress response pathway with the sulforaphane-related research going on at the same institute Johns Hopkins.
  • 00:05:06 - why cruciferous vegetables bother to create isothiocyanates in the first place.
  • 00:07:26 - the involvement of the heat shock proteins, in addition to the increased activity of Nrf2, as an additional cellular response mechanism that's been observed in association with sulforaphane.
  • 00:08:11 - how sulforaphane affects a diverse array of biochemical processes from glutathione synthesis to elimination of reactive oxygen species and detoxification of harmful compounds, including carcinogens.
  • 00:15:01 - whether or not to cook your cruciferous vegetables.
  • 00:15:34 - the epidemiological (associative) evidence that cruciferous vegetable consumption may help reduce the risk of cancer.
  • 00:18:30 - the extremely unpredictable nature of endogenous conversion of glucorapahanin (the precursor) into sulforaphane between person to person.
  • 00:22:14 - practical information surrounding supplementation of sulforaphane.
  • 00:27:05 - the effect one particular french sulforaphane supplement had on the doubling rate of PSA, which is a marker for prostate cancer recurrence in prostate cancer patients.
  • 00:28:17 - the role that the Cullman Chemoprotection Center at Johns Hopkins has played, in addition to fundamental research, in providing early, vital infrastructure enabling some of the efforts of the international research community in elucidating the effects of sulforaphane and related compounds and the underlying biological pathways.
  • 00:28:26 - the incredible, almost geometric growth in new studies that has occurred since the advent of a few of the key discoveries about sulforaphane and its method of action.
  • 00:32:48 - the practicality of probiotics as a way to improve endogenous myrosinase activity needed to convert the precursor to sulforaphane into the bioactive sulforaphane.
  • 00:33:26 - the involvement of our gut bacteria in our ability to convert the precursor of sulforaphane into its active form.
  • 00:37:13 - whether or not endogenous myrosinase activity improves as a function of repeated challenge with glucoraphanin (the precursor to sulforaphane).
  • 00:39:30 - why probiotics may vary in their degree of efficacy.
  • 00:43:00 - why consuming isothiocyanates to reduce the number of bacterial colonies of h. pylori, a risk factor for peptic ulcers and stomach cancer, may turn out to be a better intervention than complete eradication of the species with antibiotics.
  • 00:47:21 - the bizarre relationship h. pylori has with childhood asthma, where it has been shown that having some h. pylori seems to reduce asthma incidence in childhood.
  • 00:52:28 - the effect sulforaphane has on inflammation and why inflammation is often a great therapeutic target for many different diseases, including diseases of aging.
  • 00:54:05 - the life extension properties broccoli has been shown to have in an insect model of aging.
  • 00:59:27 - the underlying causes of Hutchinson-Gilford progeria and the promise sulforaphane may hold for this disease of rapid aging.
  • 01:09:00 - the effects of sulforaphane or Nrf2 activation on diseases of the brain, such as autism (human evidence) and Alzheimer's (animal evidence), possibly through anti-oxidative or anti-inflammatory effects.
  • 01:11:09 - the so-called autistic fever response whereby autistic patients report a sudden reversal of symptoms during brief periods of fever.
  • 01:10:05 - the role heat shock proteins might play more broadly in the prevention of certain neurological diseases.
  • 01:19:00 - the challenges inherent in clinical trials where scientists may be extremely optimistic about the effects that might be observed, but still have to exercise caution and choose trial conditions that may be conservative, for the good of the people whose lives and hopes hang in the balance.
  • 01:27:01 - the role of inflammation and depression and what some studies on animals have demonstrated in terms of sulforaphane's potential as an antidepressant.
  • 01:42:30 - a special isothiocyanate-containing plant known as Moringa or sometimes referred to as the drumstick tree or the horseradish tree.
  • 01:46:32 - Dr. Fahey's inadvertent foray into the consumption of exotic meats during a visit to Africa.
  • 01:51:15 - a compound commonly associated with broccoli: indole-3-carbinol and its downstream product diindolylmethane (DIIM).
  • 01:57:00 - the practicality of using mustard seed powder as an extra source of myrosinase, possibly for your cooked cruciferous vegetables.
  • 02:00:13 - whether or not it makes sense to freeze broccoli sprouts in order to extend their shelf life, and possibly even increase sulforaphane within certain contexts.
  • 02:05:25 - Dr. Fahey's thoughts on where endogenous conversion of glucoraphanin occurs in the body, as well as how long it takes before sulforaphane metabolites hit the bloodstream after ingestion.
  • 02:07:25 - Some general thoughts on frequency in terms of how often one might need to take sulforaphane to elicit its biological effects.
  • 02:12:16 - why sulforaphane may one day be a component of sunscreen.
  • 02:12:31 - what some of the upcoming trials involving sulforaphane are at the Cullman Chemoprotection Center.
  • 02:17:07 - the incredible way in which a sulforaphane-rich broccoli sprout beverage was shown to dramatically enhance the detoxification of benzene through excretion: one study showed up to 61% starting immediately after supplementation.


Podcast:  http://podbay.fm/show/818198322/e/1483675653?autostart=1

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Sibiriak, Re. Di Pierro, I didn't know him. After 1:30 minutes he ahs already said something interesting, that is the ratio Curcumin/piperine is what matters, it should be 100/1. Of course that's in extracts, it would be impossible to adjust in foods.


Re. Jed Fahey, that's an awesome interview, I remember I listened to it on the round trip commute to work, but I shoudl listen again... I'll tell you that it seems pretty work-intensive to get sulphoraphane from broccoli, although I try to eat some myrosine together from arugula from example. That's probably an anti carinogen on which a person will specialize eating, like Rhonda Patrick.

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  • 4 weeks later...

Very interesting study mechanism, sure worth of a lenghty discussion and thanks to alPater for providing such material.


My thoughts:


As far as Pca is concerned, the evidence is classified as 'suggestive' (class III on 4 classes) only for dietary Ca and selenium (higher vs lower intake).


Dietary Ca may be interpreted as a proxy for dairy products, although dairy products themselves exhibit only weak evidence of a greater risk and whole milk surprisingly exhibits weak evidence of a decreased relative risk.


These conclusions are based upon a few epidemiological studies, which although attentively selected may carry some bias. The observation of whole populations (like the blue zone but also the asiatics) with their originally low incidence of PCa may be more elucidating as to the cause of lesser prevalence. Maybe soy in itself is not a positive factor nor dairy products are a negative factor but synergistic aspects govern. The interpretations may be numerous.


Randomized controlled trials unfortuantely have the inherent problem that the sample size cannot be large for economic reasons, so in cases where the actual prevalence of cancer is low in absolute terms (as it usually is luckily) it can randomly not be verified in the study.


If we take the Theodoratu et al. conclusions literally we might as well throw away all our strategies to fight Pca and maybe eat less Ca (dairy?) and more Se (brazilian nuts), that's all.


But I believe we are all convinced that's not all...

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  • 4 weeks later...

Beetroot phytochemicals may  have significant anti-cancer effects.


Cytotoxic Effect of the Red Beetroot (Beta vulgaris L.) Extract Compared to Doxorubicin (Adriamycin) in the Human Prostate (PC-3) and Breast (MCF-7) Cancer Cell Lines




Epidemiological, human and animal studies indicate that regular use of certain synthetic and naturally occurring compounds as dietary supplements has the potential to reduce the risk of cancer [1-8]. In a search for cancer chemopreventive agents among the natural colorants and related products of biologic and synthetic origin [9], we recently identified the extract of red beetroot (Beta vulgaris L., family, Chenopodiaceae), the FDA approved red food color E162, as one of the most potent chemopreventive agents encountered in our screening [10, 11]. In commerce, the red beetroot extract is also known as “Betanin” named after its constituent, betanin (1), Fig. (1), which is primarily responsible for its red color. 


Of particular significance is the wide spectrum of antitumor  activity exhibited by the red beetroot extract [10-12]. It consistently reduced the incidence of experimental tumors in skin [10, 11], lung [10], liver [11] and esophagus [12] in various laboratory animal models. These results encouraged us to further explore the potential of the red beetroot extract as a novel natural product with chemopreventive and/or chemotherapeutic activity in combating human cancers [13].


We now report its cytotoxic effect in the androgen independent human prostate cancer cells (PC-3) and the well established estrogen receptor-positive human breast cancer cells (MCF-7)...


[...]Our earlier studies [10, 11] concur with the currently prevailing consensus that betacyanins are most likely the primary and potent anticancer constituents of the beetroot extract [1, 3, 12, 35, 36]. The present study further narrows it down and points to betanin, the predominant (up to 95%) beetroot betacyanin, as a prime candidate responsible for the chemopreventive activity of the extract.


For an overview of beetroot health effects, phytochemical bioavailability, etc.  see:


The Potential Benefits of Red Beetroot Supplementation in Health and Disease


PMCID: PMC4425174

I was unaware of the interesting process by which dietary nitrate  is reduced to nitric oxide:


Beetroot’s effect on the vasculature is largely attributed to its high inorganic nitrate content (250 mg∙kg−1 of fresh weight; [17]). Nitrate itself is not considered to mediate any specific physiological function; rather, nitrates beneficial effects are attributed to its in vivo reduction to nitric oxide (NO), a multifarious messenger molecule with important vascular and metabolic functions [14,18].
The generation of NO via nitrate involves a series of sequential steps that have been well described in the literature [4,19]. Briefly, ingested nitrate is first absorbed through the upper part of the small intestine into the systemic circulation [4,15]. It is then estimated that 25% of the circulating nitrate enters the entero-salivary cycle where bacterial species located at the posterior aspect of the tongue bioactivate or reduce salivary nitrate to nitrite [16,19]. Because salivary bacteria facilitate the reduction reaction that converts nitrate to nitrite, spitting out saliva or taking oral anti-bacterial treatments, like dental mouthwash for example, has been shown to diminish nitrate-nitrite conversion [10,18]. Under normal circumstances, however, salivary nitrite is re-absorbed into the circulation via the stomach where it is metabolised to NO and other nitrogen oxides by a variety of reductase enzymes [4,10,13].


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Very interesting find, which would suggest to include more beetroots into the diet. I couldn't find any specific betanin supplements (there is betalain though and beet root powder). Here it's very common in supermarkets to find already boiled beetroots buty some of'em are disgustingly sweet.

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Beets are a mainstay in the Russian diet--borscht, for example--but I'm not too fond of cooked beets.   I've been pushing myself to eat them more regularly,   so I add them raw into salads, or juice them raw (and combine with carrot etc. juice).  I also keep around some freeze-dried beet juice powder which is only mildly sweet and convenient to use.

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MMmmm..., I consulted some Borscht recipes and they sound and look pretty good. I'm pretty discouraged by the time required though, maybe I'm going to modify the recipe into some extra quick version with uncanned or bagged boiled beets (which are very common in Italy and parts of Europe). Or maybe I'm going to take the time and do that during a week end. Uncanned beets are not easily found here.


Last winter I baked sliced fresh beets and then marinated them for a little while in EVOO and vinegar plus capers, they were delicious, that's going to be replied for sure. 

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  • 1 month later...

A kind of a mixed message here. Look at 1:09 - 1:17 - consumption of F&V high in lycopene, such as tomatoes was not protective at all. A bust. Yet, at 4:35 - 4:41 he says the best protection is from "whole plant foods". In fact, the only point at which food (possibly due to lycopene) was protective was outlined in 1:21 - 1:27 - was processed food like pizza and concentrates, mind you, not WHOLE plant food, but PROCESSED CONCENTRATES such as tomato sauce or paste 1:51 - 2:17. In fact the more processed, the better the result, as it took 1/4 cup of tomato sauce but only 1tbsp of tomato paste which is more concentrated. So much for "whole plant food". 


Gordo's characterization is correct - lycopene extracts, supplements etc. - NO. Tomato paste - YES. 


Dr. Greger's characterization is wrong - whole plant foods - NO. Processed tomato product - YES.


Now this pertains to prostate cancer, and is based on the evidence presented. What the reality is, who knows - tune in for the next study which will debunk what happened before and we're back to square one... ain't that the way of all dietary studies? Perhaps yet again - individually tailored diets are the only ones that make sense. What works for the guy who cured his PC with tomato paste, might hasten the demise of somebody else with PC. For example, my genetic info as processed through Promethease claims I should avoid nightshade plants - such as tomatoes. Indeed, I am mildly allergic to canned tomato products, which I observed long before the whole lycopene hype. Yet again, YMMV, different strokes for different folks, there's no one size fits all when it comes to diet (or exercise). 

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The follow up video is below.  Describes a study that compared yellow vs. red tomatoes (red won).  I'm not hung up on whole foods, but tomato paste is minimally processed, most brands are nothing more than boiled down tomatoes with nothing else added.


I'm still not convinced about the whole personalized diet vs. general recommendation outside of allergies like the one you describe.  Sure if you have an allergy to nightshade plants, or fish, or nuts, obviously you'll want to tweak your diet around those things.  But things like "blood type diet" have been debunked, the whole idea of a special need for meat has been mostly debunked although still controversial in some circles.

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I'm still not convinced about the whole personalized diet vs. general recommendation outside of allergies like the one you describe.


Have you seen the link I posted in another thread:




Personally, I find it pretty convincing. It's just the first steps, but I think this is a very promising direction.

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The main jist of this is that besides already having a damaged body (pre-diabetic or diabetic, or some other disease) the gut biome has a big influence on health, digestion, and what spikes your blood glucose levels. OK, got it, but I'm not sure I agree with the conclusion. Sure you can figure out based on your current biome what foods are less likely to spike your BG. Or you could do the "Living the CR Way" thing and just not eat any high GI foods to begin with. But your gut biome is constantly changing, so this is an ever moving target, even people right here in this forum have sent samples to ubiome and seen big variation from sample to sample. And where does he think the gut biome comes from anyway? It comes from what you eat! This is circular logic. What about optimizing your gut biome? I would think eating a diverse, high fiber, plant based whole food diet with a bunch of fermented foods and pre-biotics (inulin-fos) is going to result in optimal gut bacteria (although more research needs to be done to know for sure what optimal gut bacteria even looks like). From the point of already having "optimal gut bacteria" I think you can still have a generally recommended diet. I do like the idea of tracking BG after meals to tweak what you are doing, I did this myself for quite a while. If your results from this guy's future service says you should eat more ice cream, maybe you really just need to fix your gut biome instead of eating something that is likely to shorten your life :unsure:. And he didn't directly even discuss the best approach to actually prevent or cure diabetes in the first place. Are any of the diets recommended by his suggested analysis actually going to cure the patient?


A plant-based diet for the prevention and treatment of type 2 diabetes.

The prevalence of type 2 diabetes is rising worldwide, especially in older adults. Diet and lifestyle, particularly plant-based diets, are effective tools for type 2 diabetes prevention and management. Plant-based diets are eating patterns that emphasize legumes, whole grains, vegetables, fruits, nuts, and seeds and discourage most or all animal products. Cohort studies strongly support the role of plant-based diets, and food and nutrient components of plant-based diets, in reducing the risk of type 2 diabetes. Evidence from observational and interventional studies demonstrates the benefits of plant-based diets in treating type 2 diabetes and reducing key diabetes-related macrovascular and microvascular complications. Optimal macronutrient ratios for preventing and treating type 2 diabetes are controversial; the focus should instead be on eating patterns and actual foods. However, the evidence does suggest that the type and source of carbohydrate (unrefined versus refined), fats (monounsaturated and polyunsaturated versus saturated and trans), and protein (plant versus animal) play a major role in the prevention and management of type 2 diabetes. Multiple potential mechanisms underlie the benefits of a plant-baseddiet in ameliorating insulin resistance, including promotion of a healthy body weight, increases in fiber and phytonutrients, food-microbiome interactions, and decreases in saturated fat, advanced glycation endproducts, nitrosamines, and heme iron.


(emphasis mine)

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GI foods to begin with.  But your gut biome is constantly changing, so this is an ever moving target, even people right here in this forum have sent samples to ubiome and seen big variation from sample to sample. And where does he think the gut biome comes from anyway?  It comes from what you eat!  This is circular logic. What about optimizing your gut biome?


That's not how I see it. I approach it as a black box problem. The body is a black box. I only control input, and I measure output - what goes on inside the box I am completely agnostic about. To be perfectly honest with you, I think it's the sole correct way of viewing it. You put stuff in, and you measure outcomes. Sure, you can speculate about how the black box works inside, but that's always speculation - physiology is incredibly complicated and multi-variable dependent, and theories of what actually is happening are constantly being overturned. So the only honest thing you can say is "current speculation says theory X is correct" - which says nothing about what might come tomorrow with theory Y. It's what MR calls "mechanistic speculation". So I prefer to skip all that, because it's bound to be wrong on some level. How does that translate here?


Well, I don't worry about what is responsible for this effect or that effect - microbiome, or exercise, or meditation or whatnot. That's speculating on what is happening inside the black box, and likely will be proven wrong tomorrow - the thing about science is that theories evolve. So I DON'T speculate or worry about what's responsible - if it is the microbiome or whatnot. So too with the text you bolded "Multiple potential mechanisms underlie" - why should I worry about "potential" mechanisms at all, why speculate? It's bound to be inexact and possibly wrong. No point, as far as I can see it.


Instead, I just measure inputs and outputs outside of the box, where I don't have to speculate. In this case, I can clearly describe and measure inputs - the food I consume (diet) - it is plain, no speculation needed. I can then observe the outcome - blood glucose - again, plain, no need to speculate (as long as the sensor measurements are accurate). Now, from what I understand, they tried a variety of diets and foods and measured the outcome in BG. That's good enough. I don't need to know it's the "microbiome" that's responsible or perhaps voodoo. I don't care either. I just want good outcome (BG). It avoids the bumblebee problem (the anecdote being: "physicists in the 1800's applied their theories to a bumblebee and pronounced that according to their understading of physics, the bumblebee could NOT fly; but the bublebee didn't know their theories, so it flew anyway"). By avoiding any speculation as to how the black box works, I allow the bumblebee to fly. So too here. I don't know why food X works for Bob, but is poison for Fred (as measured by BG) - and I don't care. Maybe it's microbiome, maybe not.


I mean, if tomorrow it was shown by experience that eating rocks allows you to live to 200  years of age (input: ROCKS - output: 200 YEARS lifespan), do you really care how that happens, or do you eat rocks - I eat rocks. In other words, I allow the bumblebee to fly and I don't convince myself that because it doesn't fit my theory of physics, the bumblebee doesn't fly.


Results count. That's all that matters. Sure, there may be academic interest in the "why", and I do have that intellectual curiosity, but I am much more practically oriented - I want results


And that's what we have here - concrete foods result in good outcomes. Now, obviously, you want to broaden the criteria as much as you can (what you measure as outcome), far beyond just BG, but the point stands - it's the results that count. If they got a diet for me that works to get me good measureable outcomes, that's all I care about.


What about optimizing your gut biome?


Who cares? Do I get a good measurable outcome? Yes? Then I don't care how "optimized" it is, or not.


And where does he think the gut biome comes from anyway?  It comes from what you eat!


Who cares where it comes from? Is the measurable outcome good? Yes? Then that's all I care about. 


Concentrating just on inputs and outputs avoids hanging yourself up with useless speculation - because what if microbiome is only one factor and it works in a very variable dependent way? There is a thread here on one of these forums, that Dean started, wherein he observed that a given profile of bacteria that work apparent wonders for people in Africa, are deleterious in Europeans, and the other way around. So much for "optimal microbiome". There may be no such thing. There may be instead something else - a given profile of microbiome is good for YOU, but not for Bob. For an African, but not for a European, for ME but not for YOU. And so on. Perhaps it depends on how your physiology interacts with those particular bugs - good for some, bad for others. See? So rather than speculate about the black box. I just ask a simple question: what works for me that can be clearly measured?

That's why I say: individualized medicine for the win - individualized diet and exercise program for the win. There is no one size fits all. The bumblebee flies, and that's a fact. Why, I leave to the philosophers.

Edited by TomBAvoider
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My theory is that if your starting point is a large group of unhealthy people with suboptimal gut flora that suddenly get serious about and take action toward optimizing their biomarkers of health (including BMI and post-prandial and fasting BG, CRP, LDL, HDL, blood pressure, heart rate variability, and IGF-1) that over time:


A) Gut biomes will change substantially.

B) BG response will change substantially.

C) Food choices associated with the best outcomes will converge instead of remaining highly individualized, for people that have achieved optimal biomarkers of health.

D) The food choices that result from this experiment will be similar to what has already been documented in large cohort studies of the longest lived people groups in the world.

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C) Food choices associated with the best outcomes will converge instead of remaining highly individualized, for people that have achieved optimal biomarkers of health.
D) The food choices that result from this experiment will be similar to what has already been documented in large cohort studies of the longest lived people groups in the world.


I don't believe that. I do believe that it's possible that there might be some groups of people (f.ex. Okinawans, Sardinians, X) for whom the diet might converge to a large degree, but that may very well be due to the fact that you are dealing with people of a similar genetic background. This is hardly a stretch - after all, certain ethnic groups are capable of breaking down lactose - that may work for them, but would definitely be a problem for lactose intolerant people outside of that ethnic group. We know that East Asians by and large have a very different response to alcohol. Tons of such examples. Furthermore, we do know for a fact that f.ex. Eskimos (or whatever the current PC term is - First Peoples?) have a distinct physiological reaction to their diet that is not replicated elsewhere - again, a distinct group with a distinct diet is internally converged, but not applicable across humanity. These differences are pretty extensive (see f.ex. Tibetans). So I agree that for a specific group, diet might converge, but I reject that this is true for a random human.


Furthermore, we know for a fact that different genetic profiles have a different response to diet - there's a thread somewhere here where Dean dug up SNPs which depending of the variation, F&V which are the gold standard of healthy diet, are *wrong* for some variants of SNPs (which I happen to have), and which also indicate that consuming *more* than the average of 2 drinks per day limit for men, is actually associated with better outcomes for those SNPs (which I have - good for me, as I enjoy red wine). Those are very dramatic differences.


In fact, such individual differences account for puzzling phenomena such as the great individual diet differences between centenarians and supercentenarians who don't belong to any particular group - random people across the world, dramatically different diets, yet all live to extreme old age. What explains that, if there is only one optimal diet? Clearly, there isn't. Instead, one diet works for one person, another for another person. I also know for a fact that many biomarkers don't respond in the same way to diet - f.ex. at some point Paul G. reported on his various blood sugar readings after various foods (f.ex. brewers yeast spiked for him) - and I remember that it absolutely did not work like that for me, my foods were very different. Yet both of us were on low calories and lived generally considered healthy lifestyles for a very, very long time (many years). I also know that when people report that eating this or that had an impact on their lipids, that is drastically different for me. I have moved heaven and earth in the respect of diet, and I can't get my LDL below 120 or so, yet others report minimal changes in diet components and dramatic impact on their LDL. We are just different, and that's a fact.


So I dispute that there is a single optimal diet that will have the same impact on biomarkers in all people - that is demonstrably not so. In fact there is a dramatic difference in how people's biomarkers respond to diet. And I do NOT believe that a roughly similar diet will have a roughly similar effect on different groups of people, although it might for specific genetic groups. If you are an African from the Kalahari, your diet might be the exact opposite of what works for me, someone of Scandinavian background, although granted, your optimal diet may be very similar to your fellow Kalahari bushmen - stands to reason, you share a genetic background.


Bottom line - I believe that the response to diet is very individual depending on your genes and perhaps interacting with other lifestyle factors (such as exercise).


We know for a fact that people respond differently to medical drugs - and often we can specify by percentage of population. We know for a fact that people respond diferently to exercise and many, many other lifestyle factors. It is highly counter-intuitive to then claim that somehow this one category of diet is exempt from this variability, especially given how big an impact diet has on physiology. Instead, it seems highly plausible that just as with everything else, diet too has an individual response.

Edited by TomBAvoider
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I'm still not convinced about the whole personalized diet vs. general recommendation outside of allergies like the one you describe.


Have you seen the link I posted in another thread:




Personally, I find it pretty convincing. It's just the first steps, but I think this is a very promising direction.


TomB, where is that thread? I didn't have time to answer previously and now that I can I can't find the thread. I remember there was another thread on an article which was probably authored by the same team.

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This was the article previously posted, I believe:


[1] 1. Cell. 2015 Nov 19;163(5):1079-94. doi: 10.1016/j.cell.2015.11.001.
Personalized Nutrition by Prediction of Glycemic Responses.
Zeevi D(1), Korem T(1), Zmora N(2), Israeli D(3), Rothschild D(1), Weinberger
A(1), Ben-Yacov O(1), Lador D(1), Avnit-Sagi T(1), Lotan-Pompan M(1), Suez J(4),
Mahdi JA(4), Matot E(1), Malka G(1), Kosower N(1), Rein M(1), Zilberman-Schapira
G(4), Dohnalová L(4), Pevsner-Fischer M(4), Bikovsky R(1), Halpern Z(5), Elinav
E(6), Segal E(7).

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