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Quick question: is anyone aware of any undesirable effects on nutrition/micronutrients by blending all of the ingredients in my smoothie?? (Rolled oats, walnuts, almonds,  blueberries, raspberries, flaxseeds, taurine, creatine)

I’m wondering if there is anything ‘obvious ‘ such as with broccoli, mashing it up would immediately mix myrosinase and glucoraphinin to form the unstable sulforaphane... which would not be effective if not consumed very quickly.

Thank you,

Clinton

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 When I started testing my blood glucose I learned that smoothies spiked my bg worse than the same ingredients eaten whole.  I gave up smoothies and then I gave up the bananas, mangoes and everything else with much impact on my bg.   But I was nearly diabetic as is typical for people with my muscle wasting disease and this probably isn't an issue for you and the ingredients you've listed.

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Clinton, if you find that taking a smoothie is more convenient for any reasons, then you might run a blood sugar check on yourself, as many users of these boards do and I myself have done.

That is, you can buy a relatively cheap glucometer used by diabetics with a thin lancet and monitor stripes and check the following:

  1. blood sugar before meal (fasting)
  2. blood sugar after 30 minutes
  3. blood sugar after 60 minutes
  4. blood sugar after 120 minutes

The above done in the two conditions:

  •  meal with whole foods
  • meal with foods combined in a smoothie

Of course you shouldn't exercise prior to and just after the meal.

If the blood glucose values relative to the 'smoothie' conditions are significantly higher than the 'whole foods' condition, then you have evidence that the smoothie has some detrimental effects.

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3 hours ago, mccoy said:

Of course you shouldn't exercise prior to and just after the meal.

Or test that too.  In my case I find exercise has a significant impact on blood sugar.  It has shifted me from eating once or twice daily to eating 4 small meals daily each immediately followed by physical activity.

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18 hours ago, Todd Allen said:

Or test that too.  In my case I find exercise has a significant impact on blood sugar.  It has shifted me from eating once or twice daily to eating 4 small meals daily each immediately followed by physical activity.

I started to practice that as well, in consideration of other posts, Dean Pomerliau's experiences, my own measurements and so on. 

I absolutely try to do whatever exercise after ingesting a carbs rich meal. Even squats or running from one office to the other in the long corridors of my jobsite. People know me as an eccentric guy anyway.

Yesterday I had a snag though. Since I had to go to the gym, I treated myself with a large cup of tea with 3 tablespoons of honey just prior to leave. But I had a phone call and a problem that caused me to hit the gym 2 hours later, so I just had to withstand that inevitable glycaemic peak, which by the way I ddin't feel at all and didn't compromise my workout. Once in a while maybe a significant glycaemic peak may constitute a favourable hormetic stressor!

Edited by mccoy

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4 hours ago, mccoy said:

inevitable glycaemic peak, which by the way I ddin't feel at all and didn't compromise my workout. Once in a while maybe a significant glycaemic peak may constitute a favourable hormetic stressor!

Or it may be a silent killer like hypertension which also degrades the glycocalyx.

Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that cause atheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia

...

These studies are evidence that the glycocalyx plays a crucial role in cardiovascular system health.

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In the same wiki voice, oxydized LDL cholesterol is also cited as another possible insult to the glycocalix.

But I strongly doubt that a single meal made up of saturated fats will constitute a serious hazard. Even as a single high glucose peak.

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18 hours ago, mccoy said:

But I strongly doubt that a single meal made up of saturated fats will constitute a serious hazard.

Probably not, especially if the saturated fat intake is not in the context of a hypercaloric diet and elevated insulin.  In which case saturated fat robustly elevates HDL and improves the LDL profile - large particles, little oxidation.  Here's a graphic from a study suggesting this puts one at lowest risk for CHD.

Apolipoprotein B and non-high density lipoprotein cholesterol and the risk of coronary heart disease in Chinese

Edited by Todd Allen

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On 8/29/2018 at 8:19 PM, Gordo said:

your description mentions melatonin, sleep mask, and ear plugs - to me this seems like a possible red flag

Why does this seem like a possible red flag? A red flag of what?

On 11/7/2018 at 5:38 AM, Todd Allen said:

Probably not, especially if the saturated fat intake is not in the context of a hypercaloric diet and elevated insulin.  In which case saturated fat robustly elevates HDL and improves the LDL profile - large particles, little oxidation.  Here's a graphic from a study suggesting this puts one at lowest risk for CHD.

Apolipoprotein B and non-high density lipoprotein cholesterol and the risk of coronary heart disease in Chinese

This is a graph risk of CHD per TC:HDL vs. apoB  count in a single study, not a graph of CHD risk per saturated fat intake, with or without insulin — let alone as part of a well-done meta-analysis of such findings. It's also not by itself very generalizable, even for what it says, since it has the highest apoB tertile (with low TC:HDL) having lower risk than those with lower apoB and the same TC:HDL.

You also seem to be assuming (as is often said) that increasing  SaFA will improve TC:HDL , which is an oft-repeated claim — but isn't true. TC:HDL improves when SaFA is replaced with MUFA or PUFA— though it is either worsened or held neutral by replacement with carbohydrate,(1,2) which latter doubtless will depend at the margins on the specific carbohydrate food, the specific mix of saturated fatty acids, the rest of the diet, and the immediate metabolic state.

It's also not true that increasing SaFA intake with improve the "LDL profile" (by which you mean particle size): particle size is a distraction, being a crude surrogate for discordance between LDL particle number and LDL cholesterol, as eplained here. It tells you nothing in itself about risk of atherosclerosis, and certainly nothing mechanistic.

Saturated fat really is bad for you; additional evidence on saturated fat.

References

1: Sacks FM, Katan M. Randomized clinical trials on the effects of dietary fat and carbohydrate on plasma lipoproteins and cardiovascular disease. Am J Med. 2002 Dec 30;113 Suppl 9B:13S-24S. Review. PubMed PMID: 12566134.

2.  Mensink RP, World Health Organization. Effects of saturated fatty acids on serum lipids and lipoproteins: a systematic review and regression analysis. World Health Organization.

 

 

 

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2 hours ago, Michael R said:

Why does this seem like a possible red flag? A red flag of what?

The most common reason for using melatonin supplements is to encourage sleep when sleep problems exist, the additional mention of using a sleep mask and ear plugs add to this concern (potential lack of deep sleep and/or proper sleep environment).  Sleep problems are a red flag indicating long term health and longevity are at risk.  Maybe taking a melatonin supplement and wearing masks/plugs is just as good a method as alternative ways of improving sleep, I don't know, but suspect not:  

image.png.c61ed5329c3c3040055fd945d6cdf5d1.png

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4 hours ago, Michael R said:

since it has the highest apoB tertile (with low TC:HDL) having lower risk than those with lower apoB and the same TC:HDL

But IF this is accurate it turns common wisdom upside down that lower LDL is always better.  Therere are plenty of studies showing PUFA and MUFA while raising HDL tend to have a neutral or negative effect on LDL.  Studies have also shown a very concentrated source of SAFA, coconut oil (and isolated SAFAs such as lauric acid) more robustly raise HDL than PUFAs and MUFAs and also raise LDL.  So yes, not as effective for improving TC:HDL, but perhaps a better choice for getting in the highest tertile of both apoB and TC:HDL.

 

Edited by Todd Allen

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43 minutes ago, Todd Allen said:

But IF this is accurate it turns common wisdom upside down that lower LDL is always better.  Therere are plenty of studies showing PUFA and MUFA while raising HDL tend to have a neutral or negative effect on LDL.  Studies have also shown a very concentrated source of SAFA, coconut oil (and isolated SAFAs such as lauric acid) more robustly raise HDL than PUFAs and MUFAs and also raise LDL.  So yes, not as effective for raising TC:HDL, but perhaps a better choice for getting in the highest tertile of both apoB and TC:HDL.

It would indeed turn common wisdom upside down that lower LDL is always better — particularly LDL-P rather than LDL-C — but one study does not overturn the massive body of evidence underlying the common wisdom. It's well-established that lower LDL-P is always better, at least as far down as 70 mg/dL LDL-C/700 nmol/L LDL-P , with suggestions that 50/500 is safe (provided, of course, that you aren't doing it via something that is itself bad for you, like giving someone Alzheimer's disease): it's the very driver of atherosclerosis — everything else is modification of that core effect. We also have strong evidence that replacing SaFA with plant-based MUFA or mixed (and likely even omega-6 PUFA) lowers your risk, and that raising either apoB or TC:HDL is bad for you.

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54 minutes ago, Gordo said:

The most common reason for using melatonin supplements is to encourage sleep when sleep problems exist, the additional mention of using a sleep mask and ear plugs add to this concern (potential lack of deep sleep and/or proper sleep environment).  Sleep problems are a red flag indicating long term health and longevity are at risk.

Well, yes — but he's saying that with those tools, his sleep is good. So we should (ha ha) put that to rest, right?

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From Peter attia Podcast, AMA 3: from his standpoint of longevity and heathspan consultant, Dr PA, a former champion of the keto diet (no longer now) clearly advises to keep in the lowest percentiles of LDL-p, implying that LDL-p has a sure detrimental effect on CVD. There might be people who are impervious to SAFAs consumption, some others though seem to be very deleteriously affected .

Quote

What references ranges does Peter consider too broad on lab tests? [5:30]

Lipids

  • Triglycerides (TGs): reference is < 150 mg/dL (< 1.7 mmol/L)
    • Peter wants this < 100 mg/dL (< 1.13 mmol/L)
    • More stringent, but something Peter likes to see: TG < HDL-C (when measured in mg/dL)
  • LDL-P: < 1,000 nmol/L (~ 20th percentile)
  • Small LDL-P: < 500 nmol/L (~ 25th percentile)

Why so low? The reason is heart disease and atherosclerotic disease are the most ubiquitous causes of death, so why would you want to be average?

 

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Hello all - I'm curious if anyone here is supplementing with CoQ10 - if so are you taking regular CoQ10 or reduced Ubiquinol and how much per day?

Until now I've taken 100mg of kaneka Ubiquinol - webber brand however considering reducing down to 30mg of CoQ10 (Jarrow Q-absorb; decent bioavailability sinced it's mixed with some MCT).

As with any supplementation I'm pretty sure that more is not better.  My actual 'concern' with even taking 'regular' CoQ10 (and just 30mg) is it's possible anti-oxidant effects (which I am not interested in) interfering with any benefits I hope to gain from hormetic stressors such as exercise, green tea (EGCg), glucosamine and NrF2 upregulation from cruciferous vegetables.

Several years ago I started out believing that 'anti-oxidants' were something that I wanted more of until reviewing the paper regarding the increased lifespan in mice due to the mitohormetic effects of glucosamine.  In that paper the researchers noted that when coupled with NAC (N-Acetyl Cysteine - a powerful anti-oxidant) that the NAC eliminated the hormetic effects of glucosamine on the mitochondria, and with it the lifespan benefits ... at that point my perspective on exogenous anti-oxidants was to only get them from food sources ... 

The glucosamine paper is:    D-Glucosamine supplementation extends life span of nematodes and of ageing mice Sandra Weimer1,2,*, Josephine Priebs3,*, Doreen Kuhlow2,3, Marco Groth4, Steffen Priebe5, Johannes Mansfeld1,3,6, Troy L. Merry1, Se´bastien Dubuis7, Beate Laube1,3, Andreas F. Pfeiffer2, Tim J. Schulz2, Reinhard Guthke5, Matthias Platzer4, Nicola Zamboni7, Kim Zarse1,3 & Michael Ristow1,2,3

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I took 100 mg ubiquinol daily for a month, then off for a month and back on for a month and failed to discern a strong enough effect to make it worth the cost.  I still have some left and take it now only on days I do cardio/aerobic exercise which is pretty rare, about once every 2 weeks.  On those days I also take r-alpha lipoic acid another mitochondria targeted supplement with anti-oxidant properties.  I now avoid supplements with significant anti-oxidant effects on my strength training days which is pretty much every day other than those cardio days.

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On ‎9‎/‎3‎/‎2018 at 6:15 PM, Clinton said:

I recall a YouTube video by Rhonda Patrick (PhD) where she states something similar, McCoy.  I’m vague on her exact statement and will try to find the video- but it may take several days... sorry but I’m quite busy.  

She says (again this is my best attempt to recall her words) that essentially people that do resistance training can eat more protein without upregulating  mTOR or IGF-1 (not sure - or both?) due to the demands on protein for muscle tissue repair ... 

I will try to find this video to clarify the statement and reference time in the video she says this,

Clinton 

 

Ok -

What Rhonda Patrick actually said that I recalled was wrt IGF-1 (not mTOR).  This is from her interview with Tim Ferriss:

"So, high IGF-1, higher cancer risk. Low IGF-1, reduced cancer risk and even longevity. With this new understanding of the relationship of meat consumption to IGF-1 production and IGF-1’s relationship with cancer and longevity, where it even inhibits the longevity gene FOXO3, it would be very tempting and very easy to take an absolutist position and never touch meat again, putting aside all of the other reasons why someone might make such a choice.  But as I mentioned there are good aspects to IGF-1. IGF-1 has been shown to increase lean muscle and and reduce adipose tissue simultaneously, it acts as a neurotrophic factor increasing the growth of new brain cells, it prevents brain cells from dying. It’s pretty clear that I actually want some IGF-1 activity. I think this is a really important take-home with respect to IGF-1because IGF-1 has a good and a bad side but I think exercise is a way to tip the balance towards the good. Exercise, whether we’re talking about aerobic or resistance training has been shown to to lower serum IGF-1 because exercise causes our muscles to take up IGF-1. Additionally, IGF-1 has been shown, in rat studies, to cross the blood-brain barrier in response to exercise and increases neurogenesis. This also means the exercise lowers circulating concentrations of IGF-1 which means it has less of a chance to promote the

growth of damaged cells or inhibit Foxo3 in other tissues."

 

So like with all other micornutrients, enzymes, hormones, etc. there is a balance and both 'good' and 'bad' aspects to IGF-1.

Seems like one of the (many) benefits of exercise is that muscles require the IGF-1 thus removing some of it from circulation ...

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If we knew what's the optimum IGF-1 serum concentration for the various ages we'd be able to check our individual levels with such optimum.

Longo in his interview with Hyman said 140 ng/mL, but provided no age reference.

In this article, the Brazilian population is tested with the following results (no male-female differences)

image.png.1cf3b008fd64ed7b2b2238b14d8c3b7b.png

 

image.png.f59d2d2661b560ea5f565226c74be105.png

Chinese population:

image.png.2a5ff2db5e5d095a616aaf0bbd91c54b.png

image.png.e800e0bcc5bc188d60d50c27da380d4e.png

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Sorry but couldn't find in a reasonable time tables for americans or Europeans.

Anyway, the quantity suggested by Longo is the median value in Brazil and China in the age of 50-55, whereas in Arab men 140 is  the mean at younger ages (around 40), and the median would be even lower.

So, without a reference to age, the interpretation of Longo's words is not straightforward. 

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Btw, don't forget we have this thread already:

What is the ideal IGF-1 level for longevity?

https://www.crsociety.org/topic/16981-what-is-the-ideal-igf-1-level-for-longevity/

 

See also (and various links within):

IGF-1 Tradeoff: Performance vs. Longevity

November 26, 2015

https://www.crsociety.org/topic/11411-igf-1-tradeoff-performance-vs-longevity/

Trade off between Growth Hormone & IGF-1 vs Longevity

August 18, 2018

https://www.crsociety.org/topic/16865-trade-off-between-growth-hormone-igf-1-vs-longevity/

Edited by Sibiriak

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Quote

Mccoy:  Longo in his interview with Hyman said 140 ng/mL, but provided no age reference.

 

Longo in the video ( starting around  47:35):

Quote

...140 seems to be ideal, whether you're young or old.  Now it could be very old that it may not be that easy to keep 140, but in general, in the adult population, 140 seems to be ideal.

Edited by Sibiriak

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