The price is reasonable. I enrolled. The kit came in a few days. The instructions were easy to follow. The lancet easy to use and they give you 4 tries to fill the spots with a drop of blood. My results came bact in less than 2 weeks. It was 54ng/ml - the best ever result. I am taking 4000 IU of D3 each day. Before, my level was dropping on 2000 IU.

I am more than happy to be a part of this project.

What is so wonderful about grassroots health is that potentially the health data generated by the participants will further Vitamin D research. All the sponsoring MD's are the "heavy hitters" in Vitamin D academia, from the Garland brothers in San Diego, to Dr. Donald Trump in Roswell Park to Dr. Hollis in Boston.  This is a fantastic way to further preventive medicine research instead of just making a lab or supplement maker richer.

Even though we can get our level tested through our doctor/HMO network at no cost (perhaps a visit co-pay), I decided to enroll our whole family in the Grassroots Health D*Action program.  The fingerprick blood drop collection at home also easier on our son, instead of a needle/syringe blood draw at the lab.  I really feel it is important to collect enough data about Vitamin D for more research, even if there is some out of pocket expense for us.   We seem to have developed quite a bit of resistance to all the illnesses that are spreading fast around our communities, now that our D levels are up above 60 ng/mL.  

One of the issues I do have with the current state of Vit D research is that is is primarily epidemiological.  We really need to support more well-designed intervention studies so we can tease out more conclusive evidence about Vit D.

Of course, we had a laugh completing the D*Action questionnaire for my son, aged 10.  The answer option about number of falls in the past 6 months would only allow for up to 99!  Between skateboarding, soccer, and mad-man bike riding with his friends, we estimated he might have fallen as much as 250 times in 6 months!  No broken bones, though, unlike my 81 yo MIL in the UK, who got out of bed, slipped on a magazine on the floor, and suffered a hairline fracture of the tibia, requiring a full leg cast last winter, with a long recovery.  Of course, she assures me the packet of calcium powder she takes nightly in some water (supplied to the elderly by NHS) also has Vitamin D in it, so she's covered....sigh.

Nearly everyone I know from teens to seniors, discovers their level is low if they get the test - usually at the bottom of the reference range or even severely deficient.   This is true of my friends and neighbors in the San Diego area as well as my extended family in the Northeast (incl 2 teenage sisters both with levels >20 ng/mL! - one has scoliosis, a vertebra stress fracture, and spondylolithesis!).  

Other than my husband and son, who now have good D3 levels (65-80 ng/mL) due to taking 3,000 and 8,000 iU daily this winter, only my 74 yo dad also tested with good levels this winter (52 ng/mL), despite his Northeastern location, because he's now taking the amount of Vit D3 I suggested (I sent him a 6 mos supply for his birthday in September).  My dad listens to me  .  The others might, now that their results are in  .

Thank you for posting this.  I just enrolled and will report back when I receive my results.  I'm currently taking 6000 IU of D3 daily, and am very curious as to what my levels will be.

http://www.youtube.com/watch?v=0O3L77kgU24
In this video Carol Baggerly talks about Vitamin D basics.

This link
http://tinyurl.com/dfazes
takes you to the series of 45minutes vitamin d presentations by leading Vitamin d scientists that Grassrootshealth have sponsored.

They are all excellent but of particular relevance here is
Vitamin D and Cardiovascular Disease Prevention

but I think most people will be really shocked when then watch this one
Skin Cancer/Sunscreen - the Dilemma

Hi doc

I blogged about the kit the other day - http://dadrewrite.blogspot.com/2009/03/daction-vitamin-d-testing-kit.html

All in all, I have been impressed with the experience.

I just sent my first sample off today.  I was a little reluctant to use the lancet on myself, but I collected my courage, and did a much better job than the technician at my physician's office usually does (also, I am not nearly as grumpy).  I feel fortunate to have the chance to participate, and I hope at least some of the friends and family I've told about the project will join in too.  The information to be gained by this study should be very valuable, and moreover the opportunity for individuals to take advantage of this to monitor and supplement Vitamin D on their own  is a chance to take charge of a key parameter of health.  I would like to see much more of this type of grassroots health initiative.  How I wish I could find more ways to remove the government, the insurance companies, and big pharma
from between me and my pursuit of good health.

How very interesting!  I've been taking 8000 IUs since I was diagnosed with early breast cancer last year, but my level is still only 35.1, so I'm going with 10,000for a while.  Will also join this project, as I don't believe we can afford to leave our health completely in the hands of our health"care" system.

I sent for my kit. It took about 2 1/2 weeks between the time I ordered the kit and when I got my results. My level was 44. I had been taking 2,000 to 4,000 IU per day when I did the test. The one thing I believe they could improve on is how to get the blood drops. I had ordered a home cholesterol test and their method seemed a bit superior. Same lancets but they instructed you to warm your hands by rubbing and also to force the blood by pressing on your hand by applying pressure starting with your palm using the opposite hand and working your way down. Also to do this while standing up.

I've use lancets a lot for BG tests.  Before my hypothyroidism was treated, getting good blood drops for my BG monitoring was a challenge because of my chronically low temperature.  The Vit D test needs a much bigger blood drop than a BG test does, so it's crucial to prepare the hand for the test to ensure a big enough blood drop.

People with cold hands definitely need to pre-warm a hand by any means necessary before using the lancet - hot water, rubbing, heating pad, etc.   Swinging the arm in a wide 180° arc a few times forces blood into the hand by centrifugal force, then "milking" the hand, then the finger usually helps, too.

I enrolled and have just got my results - 67 ng/ml after about three months of taking 5000 iu per day, plus eating quite a lot of seafood, butter, liver and eggs (seafood once a week, about 8 oz of liver and 6 oz of butter per week in the convenient form of liver pate, and about eight eggs per week).  I had been following a moderately  low carb diet for about a year; but at the same time I started taking the D supplements I also eliminated gluten from my diet and went _really_ low carb.  I guess my vitamin D levels weren't too dusty even before I started supplementing, since I haven't had a cold since January 2008,  but I have certainly noticed an improvement in my feeling of well being since then.  Sunlight probably hasn't contributed much to my vitamin D levels: I'm 51, live in England, work inside all day, and haven't seen any real sunshine since I visited New York for a few days last August.

I think the GrassRoots Vitamin D project is fantastic - and for anyone in the UK, it's by far the cheapest and easiest way of getting  one's vitamin D levels tested.  I plan to stick with the program.

It took a day of psyching myself into lancing my own finger.  But I did it.  That wasn't the worst part of the test.  The worst part was squeezing my finger hard enough to get large drops of blood out.  

I've been taking between 2000 and 4000 IU's per day and my test came back with my level being 44 ng/mL.  Between now and my next test I'll be taking 4000 IU every day.  It'll be easier 'cause I got capsules filled with 4000 IU so I only have to take it once a day, one capsule.  I'm hoping my level will  go up a bit.  But I'm happy that my level is up from 16 ng/mL which it was 18 months ago.  And I feel better.

baldsue,

Thanks for the report that your level was 44 ng/mL after a taking a dose of 2000-4000 for some time, and especially your earlier test of 16 ng/mL.    

My first D3 test was also 44, after about 8 mos of a 2000-3000iU dose of D3, which had me wondering how low my Vit D status was prior to supplementing.  I'm guessing it could have been similar to yours, in the teens or low 20s.  Despite moving to So Cal 13 years ago, I avoided the sun for a long time after a basal cell carcinoma was removed from my nose 10 years ago.  Some aspects of my health got worse then, too.  

Lots of little things have improved much since my Vit D level has risen to 70-80 ng/mL, though I can't say for certain that D3 is the only reason.  But I do think it's a significant factor.  I take 5000iU daily now.

I've been taking 2000 IU for the last 6 months. My test came today and my level was 29... still too low. I am currently a heart disease patient with 6 stents. My HDL before stents was a lousey 33. It is now 42. I will begin today taking 5000 IU for the next six months to see if I can get my levels closer to 60, both HDL and Vit D3.

Late to the party, but I've watched a couple of these by Dr Heaney and Dr Holik.  Really great, current information on Vitamin D.  I'm glad to see all of the D-related information posted on this blog, I'm finding it very helpful.  Thanks!

Second test results:  75!!!

I've been taking 5000IU of D3.  I think I'll keep at that level of supplementation or alternate days of 4000/5000.  Or maybe I'll go 6 months at 4000 and see what my results are next March.  Not sure of the strategy to take.  Might just keep status quo.

In the last 2 years I've gone from 16 (no supplements) to 44 (3000IU supplement) to 75 (5000IU supplement)!  

And I can't remember the last time I had a cold.  It was definitely more than a year ago.  I think it was Jan '07.

Order your own D test from Directlabs.com. They will email you the test requisition and then you go to any Labcorp for the blood draw. The results can be viewed on your online directlabs account. $69 for the test.

http://healthy-vitamin.blogspot.com/2010/03/vitamins.html

People with cold hands definitely need to pre-warm a hand by any means necessary before using the lancet - hot water, rubbing, heating pad, etc. Swinging the arm in a wide 180° arc a few times forces blood into the hand by centrifugal force, then "milking" the hand, then the finger usually helps, too.

This is helpful to hear from others. After reading this blog I asked my doctor to add a Vitamin D test to my quarterly lab for hypothyroid. It was 29 and my 88-year-old Dad was 32 (we live in the Northeast).

I started bumping up by graduating up to 10,000 IU. After 4 mos, my serum level D is 54. For the first time ever my HDL is over 50 too. All other numbers (except H1AC) were perfect.

My Dad taking only 4,000 IU per day has yet to be retested.

My husband recently tested at only 20. He has same diet and his multiple has 2,000 IU in it. I asked him to add 5,000 IU per day until our next test in 3 mos.

This is a very exciting project! My mum, aged 62, just enrolled and is very happy to be part of this. Hopefully this way more information can be gathered about this epidemic and awareness can be raised even a little bit!

To think, I was cnofused a minute ago.

Haha. I woke up down today. YouÂ’ve cheeerd me up!

Hahahaha. IÂ’m not too brhigt today. Great post!

You know, I have always made the assumption that our ancestors' teeth didn't rot because they weren't exposed to refined sugars and carbohydrates. I know accessible fluoride wasn't around then, but then again, I'm hearing that even fluoride may not be the best thing for teeth or bones (or humans) anyway.  What about Weston Price's research?
Good post!
Adam

I agree with DietKing...everything I've read has indicated that dental carries were seen only after the start of agriculture. I've also read several studies that indicate that early man more likely made a big kill and then fed off it for several days....kinda like wild cats do today. I agree that it often took several days to make a kill, but once done, it fed them for more than just 1 day.

Otherwise I agree....get back to natural as much as possible and you'll fare much better.

We are very much least we are slaves to our ancestors dna.

ironic that modern "progress" intended on increasing our survival is in fact killing us. We have built an impressive civilized society but it is not really compatible with our genetics. Maybe we need a genetic software update, nature tries to update our dna by natural selection but we have done everything possible to try to stop it either because of emotions or greed. (democrats or republicans)

Just getting around to reading some of your older blog posts.

Although I'm not completely certain, it's my impression that Marcovina was a student of Professor Sally McCormick of Otago University in New Zealand.

http://biochem.otago.ac.nz/staff/mccormick/smccormick.html

Notice they both participated in this seminal article.

Sharp RH, Perugini MA, Marcovina SM, McCormick SPA: Structural features of apolipoprotein B synthetic peptides that inhibit lipoprotein(a) assembly. J Lipid Res 45:2227-2234, 2004.

I'm very certain that Rebeca Sharp was a student at Otago.

More importantly, Sally McCormick has applied for a patent mirroring the article title linked to above at wipo.int.  Don't have the link handy.

I often soak raw almonds (and other nuts) about 24 hours in filtered water with sea salt, then dry them a day or two at about 150°F in the oven.  I doubt the studies take this kind of "processing" into account, but any idea how that might change the absorption scenario?

I'm glad you posted this.  A few women I know have been wary of eating many nuts for fear that fatty nuts would cause them to gain weight.  

Really like the little bit on healthy gut flora caused by almonds too.  A healthy gut is important to me.

I would certainly agree that it is possible to eat enormous quantities of nuts without absorbing all of their calories. I noticed I could remain weight stable while sedentary and eating 3,500 calories back when I used to eat large quantities of nuts. Even when well chewed a proportion of them end up you-know-where! Just flush...

Peter

Dr. Davis, this is a great example. Thanks for posting it. I have a question on the 88 calories. I tried to work through the calculations to demonstrate this to one of my clients. I couldn't come up with 88 calories per ounce.

I kept coming up with 80 and here's how. 50% calories from fat is 63. I used 50% for protein and digestible carbs - based on the info provided. For protein, that leaves 3 gms or 12 calories. For carbs, half of 2.5 gms is 1.25 gms, which equals 5 cals. These add up to 80 (63 + 12 + 5).

I’m probably making a silly mistake but I’d like to come up with the same numbers when demonstrating this to clients – makes me feel kind of silly.

Thanks again for the blog, I greatly appreciate the information you post.

Brian

Does pasteurization affect the positive effect almonds have on gut bacteria? Last year it became manditory that all California almonds must be pastuerized by one of these methods: fumigation with propylene oxide, blanching and oil roasting. This is to prevent salmonella. http://www.almondboard.com/Programs/content.cfm?ItemNumber=890&snItemNumber=450

I eat a handful of almonds just about every day. I have wondered if there benefits have been compromised.

The study was sponsored by The Californian Almond Association

In the era of the 64-oz. soda, the 1,200-calorie burger, food companies now produce enough each day for every American to consume 3,800 calories per day as compared to the 2,350 needed for survival. Not only adults but kids are also consuming far more calories than they can possibly use. http://www.phentermine-effects.com

For a long time I've suspected that some foods are very inefficiently absorbed. I've particularly suspected that raw nuts are relatively poorly absorbed and thus yield only a fraction of the calories ingested.

Dr. Davis, would like your thoughts on the Trader Joe's brand Omega-3 Fatty Acids:
1200 mg Fish Oil
400mg EPA
200 DHA
Thanks,
Chris O

I use Pharmax Finest Pure Fish Oil with Essential Oil of Orange from the TYP Marketplace.  I take 1 tablespoon per day to help reduce Lp(a).  Is it better to take this dose at one time or divide it through the day?

In Iceland where I come from we have a really high quality fish oil called Lysi.

In my opinion liquid form is the only real way to take it, with caps you have to take a ridiculous amount to reach the same amount as in a tablespoon.

Plus you have no way of knowing if the fish oil caps are spoiled except to chew them, often they're not even refridgerated in the supermarket.

I remember from an earlier thread that spacing the dose out over the day works better than a big dose once daily. That makes sense, given that you are trying to alter some liver metabolism that goes on around the clock. I've been using the Life Extension capsules, six a day, for several years with pretty good results. It gets my TG from 400+ to about 170. I'm hoping the gram a day of regular niacin I've been taking for a few months helps further and gets my HDL out of the sewer (27). I'll know that in a few days...

Nice tasting Liquid fish oil brand, 1 teaspoon=
1,500 mg EPA
+ 750 mg DHA
----
= 2,250 mg EPA + DHA
+   380 mg other Omega 3
-------
= 2,630 mg. Omega 3/teaspoon
(out of a total fish oil content of 4,400 mg./tsp.)

Canada made "Natural Factors",
"Dr. Michael Murray recommended pharmaceutical grade" says label; extracted
from anchovy/sardine/mackerel;
1 teaspoon stateside cost works out to less than US$1 a teaspoon; each teaspoon has 40 calories, 15 mg cholesterol, total fat 4.5 gr. (being 3.5 gr. polyunsaturated), natural vitamin E and natural orange flavor, no heavy metals/environmental toxins ... I've no financial interest in the product.

What about Carlson's?



http://www.amazon.com/Carlson-Finest-Liquid-Omega-3-Orange/dp/B001LF39S8/ref=wl_it_dp_o?ie=UTF8&coliid=I27QWKFK5P760T&colid=1J0P20X13IM7F

What are your thoughts on Chris Masterjohn's research regarding very low requirements of polyunsaturated fats in the human diet?  High amounts of fish oil would certainly contravene this hypothesis.  I am referring to his position paper, How Essential Are The Essential Fatty Acids?

The best fish oils should be, as expected, in fish. Eat more fish!!!;))

"1 teaspoon Pharmax fish oil, for example, provides an equivalent quantity of omega-3 fatty acids as 6 standard fish oil capsules on a milligram for milligram basis, but more like 8 to 9 capsules when absorption efficiency is factored in."

Color me confused, Dr D. At the moment, I ingest 6 (3, 2x/day) Sam's Club Omega 3 capsules (the ones you recommended in a long-ago post) to obtain the 6 Grams of total DHA and EPA/day. Does your comment I quote above mean that, with the liquid form, I can take less than the equivalent of 6G/day  because of its absorption efficiency? And how much, if yes?

Really, I am sufficiently befuddled that I think even my question is not clear...

Help!

Where can I check if the fish oil is trigyleride form?

uh.. off topic.. when I clicked on my bookmark, to the Heart Scan Blog all of the website except these comments are in what looks like Russian!!  nothing else on my computer is corrupted...anyone else?.. and how do I fix this?  I am on an IMac.

Thanks,
Jeanne

Fixed it!  funny that it was only this website.

on topic- I am very intolerant to anchovies, will Krill oil help me?  can't take ANY fish oil with anchovy.

Thanks

Seeing some confusion here: the ideal active ingredients in fish oil are the EPA mg. & DHA mg. omega 3's. Lables indicate there are other omega 3 oils, plus other non-omega 3 oils in all products and together these are the mg of "fish oil" (product may specify yet another blending oil). Companies make their EPA mg. & DHA mg. concentrations different, incur production costs to make it higher doseage and our purchase price reflects that.

If you have a theraputic goal for intake: it is not so much how much fish oil, but how much you need to take of any one specific product a day to meet your target for total EPA mg. & DHA mg. Omega 3 fatty acids. For a name brand product Doc recommended and gave his daily dose (whether capsule or liquid)he apparently did the math.

Unfortunately I am illergic to fish oils and react badly to them. Not a good way for me to get my omegas so I need an alternative.

Udo' Oil does do a 369 oil that has no fish oils. So far that is the only one I have been able to find I can handle.

best fish oil is no fish oil. Certainly if anyone knew how fish oils were made , they would not take them. It's interesting how dr. Davis says fish oil with no odor are best but those are simply sterilized and deodorized and for a reason so that the taste of smell would not be repulsed. Trust your own gut instead of anyone else I guess. Ray Peat has chronicled data and science behind the dangers and lipid peroxidation of fish oils. Brian Peskin makes a case that these derivative oils are a huge burden for the cells and should never be taken. Naturally such oils are protected by vitamin E and saturated fat but not in these fish oils. Most other literature documents effects of omega 3 on cancer metastasis, just google it.

Now Foods Omega-3 Fish Oil 16.9 fl. oz.
Serving Size: 1 tsp (5 ml)
Servings Per Container: 100
EPA: 740 mg
DHA: 475 mg
Other Omega-3 Fatty Acids: 185 mg
Total Omega-3 Fatty Acids: 1,400 mg

Cost: $19

100% triglyceride form **

** Now Foods 16.9 fl. oz. is the brand I use and I can confirm this is the TG form after a polystyrene test.  (Take a styrofoam cup, place a small amount of fish oil at the bottom of the cup, wait ten minutes, and if it eats through the bottom it's the EE form.)  

I can also attest that I do not suffer from "fish burps" that the EE form is known to cause.

Anonymous about Lp(a)--

We have no formal data on dosing regimens, but I have been advising dividing dose in two, a.m. and p.m. This appears to be working well.

David--

You may be confusing fish oil dose with dose of EPA+ DHA.

Check your label to see EPA + DHA content. This is what you use to dose your fish oil.

Readers

Is Carlsons fish oil the Triglyceride form one?

SVinay:  Carlsons Super Omega-3 Fish Oil is the ethy ester form.

I am currently taking Heart Health Omega-3 1000mg by Swiss Natural Sources.EPA 300 and DHA 200.  I take three capsules daily.  I have also purchased Jamieson's Omega-3 Select with the same EPA DHA content as the Swiss.  The Jamieson's is less fishy smelling and I will switch back to it when I finish the Swiss.  
Canned boneless herring fillets are usually a part of my lunch.  Omega-3 2g.  I also found some canned cod liver.  I'll try it in an egg bake.

For the poster who had a question about Carlson's... the liquid and low-dose caps are natural triglyceride. Their higher concentrate capsules are ethyl ester.

I currently like Barlean's, as it's triglyceride and relatively inexpensive. Their higher concentrates are ethyl ester though, so go for the lower conc. ones if you want the trig form.

I do disagree with Dr. Davis as far as preferring liquid however, due to oxidation issues. I'd recommend the caps instead, and simply chew them, if swallowing capsules bothers you. The caps do offer some extra oxidation protection.

Hi Vlado,
I think so-called
"pharmaceutical" grade fish oil is distilled to seperate out concentrated gradients of "x"% DHA & "x" % EPA in a product. Yes, fish scraps that the oil is extracted from first gets heated, but so is cooked fish. Solvent residues concievably might be in some products; you can inform me of other compounds resistant to purifying out.

1 teaspoon oil = 5 mL. = 200 pharmaceutical size droplets = 4.54 grams .... I, for example, weigh 79,379 grams (175 pounds/79.4 Kg.) and assume a daily teaspoon dose of 4.5 grams fish oil can be metabolized safely. If you've details on how the omega 3's are noxious when added into the diet please explain.

Is my fish oil already peroxidized and/or are ingested omega 3 lipids peroxidized to my detriment at this level? My math shows that one teaspoon for me is 5.7 hundred-thousandths of my body weight; multiplying 0.000057 x 79379 grams that I weigh = 4.5 grams in teaspoon of oil.

Is there any data guiding recommendations on the ratio of EPAHA? I've never come across any primary data on the subject. To the best of my knowledge, the ideal intake and ratio of EPA and DHA remain unknown and a point of contention. I've noticed many fish oils have a 3:2 ratio of EPAHA, but I don't know where that is coming from. I'd love to know your thoughts, Dr. Davis.

I love the brand from www.strongerfasterhealthier.com
They make 5 flavors with zero fish oil taste. My kids ask for it, so it's a big win in our house. The concentration of EPA and DHA towered over even barleans.

Carlson's Super DHA Gems and EPA Gems concentrate capsules are TG form.

Dear Dr Davis

I am looking for a Kosher liquid omega 3 fis oils
I find nutri supreme research
Calories   40

Calories from Fat   40

Total Fat   4.5g    7%**

Cholesterol   18mg   6%**

EPA   950 mg   *

DHA   475 mg   *

Other Omega 3   325 mg   *

Total Omega 3 Fatty Acids   1750 mg

is this ok? or there is something Kosher better?---------------------------------------------

Check out Ascenta! All their fish oil is in triglyceride form.

ascentahealth.com

What is your opinion of Krill Oil?

Dr. Williams, I am wondering what you think of only taking high doses of EPA? See the following article:
http://igennus-hn.com/omega-3-epa-treatment-for-a-heart-condition-news-release/

As I have M.E. (post viral fatigue syndrome) as well as astronomical total cholesterol (great tryglycerides), I''m interested in trying this protocol. Would love your input.

The fixation on cholesterol is blinding the medical establishment to more significant factors, while lining the pockets of big pharma.

Of course, you and I know that there is far more to reduction of cardiovascular risk applied to a framework of serial plaque quantification ("tracking plaque"!) than statin drugs. I doubt that a man as intelligent as Dr. Grundy truly believes this. I suspect that he is simply stating what he knows what will be published without resistance in the standard medical literature, trying to achieve a modest incremental success just by raising consciousness about heart scanning and plaque imaging: first things first.

Thanks for your post and welcome to check: here.

Thanks for the information Santa. I notice that you are drinking a Coke. You should lay off of that, too.

Merry Christmas and Happy Hanukkah to fellow TYPers!!!  Here is to a successful 2008, slim Santas and if anyone sees Rudolph and his bright red nose, you might mention to him that drinking alcohol to excess raises triglyceride levels.

There isn't much vitamin D in the North Pole, is there? Rudolph's red nose could also be remedied...

But, Coke and cookies are soooo good!

Love this post! Just thought I'd say HI! I found your blog via BlogRush!

Deborah

Hi, Santa!

Thanks, as always, for your on-the-mark, pertinent information!

However, Santa, with all due respect, Santa, Christmas is o-v-e-r, so please post a new blog, perhaps pertaining to the upcoming Valentine's Day, which would be perfectly appropriate, since that special day symbolizes "hearts".

And so it goes. I'm tempted to put Santa's testimonial on our homepage, but I think that may be tooting our own horn a bit too much.

Real men aren't terrified of an entire macronutrient because of a poor understanding of science.

Then why do I have boys (later men) doubling testosterone when switching from a very low-carb to high-wheat, high-carbohydrate diet?  

http://180degreehealth.blogspot.com/2011/03/natural-testosterone-enhancement.html

Dr. Davis,

Can you explain why I remain lean eating 15 pounds of potatoes, 2 gallons of whole milk, and close to 2 pounds of butter every week? That's in addition to regular meat, eggs, other added fats, root vegetables, beans, occasional grains, and other carb sources like fruit and molasses. I'm 6'3", 175 pounds, have never dieted, and do not exercise. My weight has never gone higher than 176 pounds.

Thanks,

Mike

"Real men don't eat carbs."

Are you saying half a billion Chinese men and 70 million Japanese men aren't real men?

-DIANA

Prolactin secretion is held down by dopamine; with less dopamine turnover the prolactin self-regulation feedback loops are disturbed. Age has a role in the efficiency of prolactin receptors on the hypo-thalmic dopamine neurons.

Prolactin secretion is increased by seratonin, vasopressin, cholecstokinin, Beta endorphins, angio-tensin II, thyrotropin releasing hormone, enkephalilns Leu & Met, growth factors of epidermal and fibroblast, substance P, oestradiol 17Beta, and pituitary response to prolactin-releasing peptides.

Normal testosterone release has a  peak that inhibits prolactin for 9 -11 hours; when testosterone release is at it's lowest point in releasing cycle then estradiol gets active. Estradiol cycle is for 15 - 18 hours; and when estradiol starts to kick in the prolactin cycle of 20 - 23 hours gets going again. Estradiol in high amounts has a paradoxical effect; it lowers prolactin secretion instead of normally working toward increasing prolactin secretion.

Prolactin has a feed back loop with testosterone; it can act on the cognate receptors in the testes Leydig cells to raise testosterone. Testosterone, for it's part, can supress the synthesis of prolactin.

After the aged male ejaculation there is a secretion of prolactin that is sustained for about 1 hour; this is refractory, and if there is arousal without actual orgasm then that prolactin refraction does not occur. With healthy young males there is no post-orgasm prolactin perfusion; and thus their refractory phase is brief.

Where (in brain or in periphery) the prolactin is being considered has to be born in mind; as does the context (normal or altering). Chronic high prolactin in men is associated with poor sperm fertility.

Carb engendered insulin resistance I can see as down stream leading to more free fatty acids circulating; that, and the fact that as we age our sub-cutaneous fat cells tend to get less responsive to insulin anyway. The "freed" fatty acids cause blood albumen to release tryptophan, a substrate for synthesizing seratonin (and thus more prolactin). With age there is less need for tryptophan amino acids and so the ample western protein supply of dietary tryptophan might be a co-contributor (among others).

but who was troll?

Thanks Dr Davis for great advice as usual.

Dr Davis, have you noticed that humans somehow are arrogant enough to believe that they can eat whatever they want and still maintain good health anyway? It's like pretending a lion or cow can eat whatever it wants with no ill effect. Or maybe it's just my impression lately.

SSRI (seratonin selective re-uptake inhibitors) entail many formulations; a number of them are associated with loss of libido (reduced sex drive), ejaculatory anorgasm, +/- 25% men get erectile dysfunction  and sometimes impotence. Seratonin is a factor increasing prolactin production by the pituitary gland.

Carbohydrate ingestion is a popular  on-line recommendation to boost seratonin levels. The National Sleep Foundation states carbs make tryptophan more available to the brain; once tryptophan crosses the brain blood barrier we can then make seratonin from it.    

The journal "Public Health Nutrition" (Jan. 2007) details that our muscles will absorb amino acids except for tryptophan; the tryptophan builds up a "pool" in the blood to draw upon. When one is young &/or geneticly favored (among other exceptions) they are not plagued by the insulin resistance corollary of elevated free fatty acids causing their  albumen "pool" of tryptophan to head on toward excess seratonin synthesis.

Doc likes to post provocative snippets; not footnotes we can find by searching the internet (try "Yandex" search engine if getting poor pickings). I am not fixated personally on low/no carbs, so am not advising anyone here about diet. My unsolicited observation is that age and time often confound an individual's metabolism; what was once "great" may sometimes merit reconsideration.

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I think it would be more precise to say real men don't eat starches.  After all, vegetables are carbs, and I don't see anyone saying that veggies are bad for you....

WOW!  So much misinformation in such a short post.  

These kind of posts only undermine the nuggets of good advice you may provide.  

By your logic the human race should not even have survived agriculture!

Dr. Davis,
Please post my "Endothelial dysfunction ..." comment, your
Spam filter seems to have held it on 28th, following CarbSane's.

@Carbsane

Every statement can be verified. Which one is not true, i.e. misinformation?

As far as I can see, every one of those statements are true.

@Matt Stone

Congratulations, you have just discovered puberty (boy turns into man, doubles testosterone level in one year). You have also discovered the premature-puberty-triggering properties of wheat. It probably acts primarily through the insulin/IGF-1 pathway.

Um...actually, non-starchy vegetables are not a carb source for humans, they convert into fat in our gut through bacterial fermentation. Vegetables are actually very low in sugars. Ruminants like cows ferment grasses into fats; they are getting most of their energy from fats.

I am trying to de-program a friend that has been McDougaled.  McDougal is telling him all the scientific studies support hi-carb vegan diets.   Where can I find studies to counter these claims?  Especially about wheat.  I find Dr. Davis' articles on wheat quite compelling, but I need to show him studies.

Facts are facts.  A man with a testimony is not at the mercy of a man with an argument.    Sugar/Carbs raise insulin levels.

2 years lo carb hi fat.  30-50 carbs per day.  35 pounds lost.  Last VAP test was HDL 72, trig 52, LDL pattern A.  I'm 45 years old.  Exercise moderately.    I have discovered that FAT is your friend and sugar/carbs are the enemy.  Seems to work for me.

@Martin:  Perhaps let's start with evidence that carbs de facto  increase visceral fat.  So many of Dr. Davis' posts of late begin with either a false or unproven premise.  Some, like the recent battery acid post about oatmeal really take the cart over the cliff!

consider also: "life w/o bread" by wolfgang lutz, md, internist, wherein elevated insulin in response to carbohydrate ingestion is demonstrated to suppress testosterone and human growth hormone.  taubes also recognizes elevated insulin as a suppressant of t and hgh in gc,bc.  and sir, what a pity to see carb crank and her ilk here.  edit, please.

carb sane - why do YOU not respond to the others commenters here that are critical of your endlessly unsubstantiated comments (your nonsense, really)? Your insisting that  Dr Davis support HIS statements makes you look EXTREMELY hypocritical when you do not support your OWN statements.  

Please do better. If you do not like what Dr Davis posts, you can simply stop reading his blog, and stop making silly, inane comments (that make you look like a hypocrite!).

Dr. Davis,
Again request you to kick out of old Spam filter my  28th April post on this thread.  When I sent it your old blog format showed it in comments section right after CarbSane's 28th posting.
It  begins : "Endothelial dysfunction ...." and goes on to discuss particular  details related to  your premise that carbohydrates can contribute to male dysfunction.
I don't  have it saved to re-send and won't spend time trying to recreate it .  It wasn't "X" rated and maybe some of the  guys here might find it interesting.

CarbSane  shouldn't have to sing in the choir in order to participate and I,  for one,  hope she will continue to  comment  here.  I  request she stay on the island  ....
Unrelated:  
I just noticed this  blog format now  uses a  "Reply" to individual commentator's posts (ex: Tyson's 28th Ap. comment got a reply underneath from Steve on 29th Ap.).  Since I follow an entire thread this is annoying; because now I can't just go to the last comment I read (or date)  and keep abreast.
It's not like we are at a world events blog sounding of  on endless nuances.  Revisiting all the previous comments for   input is not  pleasant.  I will not use "Reply" and keep comments sequential,  like blog set up was before.

CarbSane has pointed out that carbs do not "de facto increase visceral fat";  she did not deny that carbs are implicated in de novo lipo-genesis.  In a sense the deal with carbs   relationship to internal fats  is location, location, location; and probably time complicates  the  functional impact.

High  carbohydrate diets increase triglycerides in the liver more than dietary fat does.  High dietary fat intake, in comparison, is what increases trigs in the plasma more readily (ie: chylomicron bound trigs) than ingested carbs.

Repeated high carb  intake can upregulate a  lipo-genesis gene, the sterol regulatory element binding protein 1c (SREBP-1c);  once  SREBP gets active this gene keys more activity of enzymes  fatty acid synthesase  and more mRNA of acetyl-CoA carboxylase .  The liver then goes on to make more triglycerides.  

A separate affect of high carb diets is the up-regulation of the enzyme pyruvate kinase, a glycolytic enzyme.  This involves the ChoRF (carbohydrate response factor) binding to a DNA ChoRE (carbohydrate response element) and then  the protein ChREBP (carbohydrate response element binding protein) complex hypes up the liver pyruvate kinase;  fostering a pre-disposition where mitochondria are set up  to burn glucose for ATP,  and not fatty acids nor ketones.

@Mito:  In humans, DNL is not a significant contributor to body fat accumulation.  It only becomes quantifiably significant in the context of massive carbohydrate OVERfeeding.  See studies linked in these blog posts of mine:  Excess carbs converted to fat?, Postprandial DNL, Nutrient Fates, Fat Futile Cycling of Carb Excesses.  

Paul Jaminet over at Perfect Health Diet had an interesting take on the subject of that last link:  How does a cell avoid obesity?.

Are high carb consuming cultures known for their moobs?

Well a priori, it's true. Carbs increase visceral fat. What makes you believe otherwise?

Actually, the opponents of the carb hypothesis always point out how fat cells always take in fat, and always put out fat. So do the proponents of the carb hypothesis incidentally. So in effect, any substance that causes fat cells to take in fat, increases fat cells. Thus, carbs increase visceral fat. De facto, sine die, that's it for that.

To say carbs don't increase visceral fat is to say carbs don't ever take a trip inside a fat cell at any time whatsoever never ever. How is that even more plausible?

Ian, since you have a better understanding of science, please explain what really happens when a man consumes "healthy whole grains".

No, a priori it's not true.  I didn't make the assertion, Dr. Davis did.  I'm asking for the evidence in support of that.  Why should I, or anyone for that matter, be tasked with disproving an assertion?  That's not how it works Martin.  To your other post, I didn't say carbs never cause fats to be deposited in visceral depots.  That would be ridiculous.  But I've yet to see evidence that they cause increased *accumulation* of fat in same.  Have you?  I'm interested in seeing this evidence.

@Mito:  It appears my response to you is in moderation limbo - links?

Here's the stripped version:  @Mito: In humans, DNL is not a significant contributor to body fat accumulation. It only becomes quantifiably significant in the context of massive carbohydrate OVERfeeding. See studies linked in these blog posts of mine: Excess carbs converted to fat?, Postprandial DNL, Nutrient Fates, Fat Futile Cycling of Carb Excesses.

Paul Jaminet over at Perfect Health Diet had an interesting take on the subject of that last link: How does a cell avoid obesity?.

Are high carb consuming cultures known for their moobs?

You sound like a sentient enough being (that's a little dig at the multiplication sentient being filter here ... not a dig on you!) to use the labels function or other search stuff to find the posts if you're interested.  All of those posts on my blog contain links to the full texts of some rather nice papers.

@Terrence:  When someone makes an assertion, the burden of proof is on them to back that up.  

@Martin:  It's pretty lame to conflate fat deposition - that we all agree occurs continually - with fat accumulation.  By your logic, everything causes visceral fat and all you fellas would be running about needing "Bros" or was that "Manziers"?  

Dr. Davis' claims all hinge on some special tendency for carbohydrate intake to lead to visceral fat accumulation.  It could be true.  I haven't seen much in the way of evidence though.

Back to Mito:  You said "High carbohydrate diets increase triglycerides in the liver more than dietary fat does."  I would point out the key word "in".  Are we talking elevated circulating triglycerides produced by the liver, or are we talking hepatic triglycerides?  Two different animals.

carb sane said "@Terrence: When someone makes an assertion, the burden of proof is on them to back that up. "
PRECISELY, carb sane PRECISELY!

Exactly WHEN will YOU "back up" your empty, meaningless assertions about Dr Davis's blog? WHEN???

Every assertion in this post hinges on increasing visceral fat.  Dr. Davis did not provide substantiation for his assertion that eating carbs does so per se.  That's his burden, not mine for pointing out his lack of substantiation.

Fat intake doesn't get a free pass;  depending on the amount (& type) of dietary fat it can contribute to obesity. At 10 - 20% dietary fat there is negligible contribution to weight;  it doesn't trigger intestinal gene expression related to lipid metabolism that promote  a metabolic syndrome.  

Constant intake of 20%  fat gets PPAR  (key lipid metabolism gene) busier; and by the time regularly consuming 30% dietary fat  gene alterations have more significant  potential to affect body weight. When the diet is 45% fat then fat absorption continues to occur even further down along in the gut as genes up-regulate there to handle the high fat intake.

Physically active people (ex: exercisers , agrarian ancestors,  hunter gatherers, youths) up-regulate AMPK  (adenosine mono-phosphate activated protein kinase); which  effectively counter-balances the effect of  regular high fat intake down-regulation of AMPK (a energy sensor in a cell when cellular energy is low) .  High fat diet retards  phosphorylation of  AMPK  gene and this stymies the mitochondrial Uncoupling Protein (UCP3);  UCP must  first activate in order to switch over to burning fat in our cells.

With AMPK down shifted the cell house- keeper recycling step of auto-phagy is inhibited; cells accumulate debris from oxidized fats and old mishapen proteins, with cell's attendant burden of ROS (reactive oxygen species, generated  from unchecked NADPH oxidase enzymatic activity).  Palmitate fat  (for example) can cause down-regulation of AMPK and downstream  activate inflammasomes (ex: NLRP3) that contribute to adipose tissue problems;  however,  adequate K+ (potassium) ions are able to nullify the inflammasome  spark.

Palmitate  (ex: lard = palmitate and oleate, et.al) generates ceramide molecules  ( a sphingo-glycolipid;   "sphingo" was an original typographical error instead of discoverers  chosen "sphinx-" prefix, relating to how molecule interacts biologically and enigmaticly flips it's own molecular orientation); ceramides work against insulin action in our muscles, and thus can contribute to insulin resistance (ie: risk of  pre-diabetes). Muscle ceramides are mostly made with the  fatty acids derived  from dietary fat;  in the muscle they (ceramides) increase insulin resistance . Oleic  acid, and other long chain fats,  get into intestine chylomicrons as triglycerides; their route is via mesenteric lymph transfer into the blood circulation at the left-subclavian vein (ie: don't go directly to liver).

So, ceramides in the liver are different because they are essentially  from de-novo lipogenesis; those ceramides are not considered to directly cause of insulin resistance. In other words,  if the individual has good insulin signalling in the liver  there is still the potential for muscle insulin signalling to be made worse by constant  high fat intake.

Lifestyle and genetics are not discussed here as mitigating factors; the dietetic strategy of eating fat to lose weight is not being parsed here .  The modern diet of abundance,  high in both fat and carbohydrates, probably  is more of a double whammy for weight gain than either die factor taken in isolation; protein is not factored in here either .

You ask why should anybody be tasked with disproving an assertion. Imagine if scientists had the same idea. Nothing would be done. If you disagree, _you_ are making an assertion. By your own logic, _you_ are tasked to prove your assertion. That's how it works miss sane.

You say it's ridiculous to say carbs don't cause fats to be deposited in visceral depots. This means you say carbs do cause fats to be deposited in visceral depots. However, you disagree that carbs cause increased accumulation of fat in same. In effect, you disagree that carbs cause any kind of dose response of the same. Now that's ridiculous.

As for evidence of all this, Gary Taubes Good Calories Bad Calories is as good a place to start as any. The key detail is insulin and the fact that visceral fat tissue is so much more sensitive to it than other fat tissue. To summarize, carbs drive insulin drive excess fat accumulation. Since visceral fat is more sensitive to insulin than any other kind of fat tissue, carbs drive more excess fat accumulation there than anywhere else. I'll try to find a more specific source for this if I can. But don't wait up, I could be late.

2 times got "server" error for comments here...this is a 3rd.
I miss the old blog set up.

Hi CarbSane,
13 women & 5 men with BMI = 35 +/-7 and fatty liver (non-alcoholic) followed 2 different diets (2011 study) for 2 weeks only. I think this might validate one of Doc's contentions; sorry comment seems brusque . (Unrelated: yesterday I  said "in" the liver, no circulating trigs were detailed ;  and  said "high" carbohydrate, whereas you classify "extreme" as game changer.)
Studied group 1, restricted calories to 1,200 & 1,500 daily for women and men, respectively. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 28 (+/- 23)%
Studied group 2, restricted carbs to maximum of 2o gr./d for both sexes and had no calorie restriction. Weight loss after 2 weeks was +/- 4.3% and circulating triglycerides dropped 55 (+/-14)%

edit correction from me CarbSane,  
The triglycerides  in low cal/low carb  diet comparison I cited were explicity  liver trigs,  and not circulating trigs as I skimmed from my notes; measurement of liver trigs was done by magnetic resonance spectroscopy.  I thought my synopsis was unlikely so  just traced the study back to Am. Jrnl. Clin. Nut.(ajcn.org/content93/5/1048); sorry about the error.

Hi, Might--

Sorry, but I can't find your lost comment. I don't know what's become of it.

I'm also just getting used to this new format.

There's much evidence that it's the lack of fat in the diet that leads to increased caloric consumption. We could still posit that it's the caloric surplus that causes obesity. But we can't discount the possibility that it's the lack of fat (and the surplus of carbs) that causes obesity, which we then compensate for by eating more, and that's what we see.

Considering many studies that show just that, that eating more fat leads to satiety which leads to eating less and losing weight simultaneously, and that hunger is an indicator of nutritional status (fuel partitioning for example: too much toward fat cells, too little toward every other cell), we can't just conclude that we grow fatter because we eat too much.

Add to this the fact that many drugs, which contain exactly zero calories, make us fatter by themselves (and some make us leaner, ha!), and it's clear that the problem can't be expressed by calories alone.

Ironically, you go on about physiological mechanisms to explain how fat can make us fat, but then proceed to posit that it could still be all about calories, i.e. abundance. Now that just doesn't make any sense to me. What's the physiological mechanism that controls "calories" then?

I enjoyed this post, but it begs the question: do real men look like Popeye?

Hi Martin Levac,
Just  saw your "reply" under my fat doesn't get a free pass comment; please tag me with new sequential thread comments (instead of as reply) to be sure I catch what you wrote.  I am not declaring excess weight gain is a clean cut factor of either  calorie, carb or fat intake;  genetics/epigenetics /age/pathology  will have a role in how susceptible one is to their  (carb & fat & protein) influence.  

I don't have  any  specific formula to promote for every one. Satiation at a meal is  well worth considering as a control  factor; unfortunately,  we are able (and many have access) to not only keep eating, but also to soon " graze" on food again irregardless of our abated hunger.

Fuel partitioning, as you mention it,  is a bit confusing to me. If your concept relates to how the body "burns" it's energy for functioning then that relates to one's underlying diet; we are set up to pump out energy in essentially distinct  mitochondrial steady states.

Our cells don't want to be oscillating , in real time, between burning fat and glucose;  slipping in & out of phase, in real time,  is normally prevented by a high threshold  that must be exceeded to switch mitochondria over to other fuel.  In this case there must be a relatively strong OFF signal needed to get out of  the already up and running mitochondria mode,  and into the ON for a different mode for burning the other fuel.  

The output of these types of cell signals (ie: Off/ On & On/Off  ) is a function of the previous history of trans-genetic activity (ex: genes key to burning fat or carbs and their respective cascades of genes that keep the process going) ; and this type of  threshold program is encoded on a chromosome  (like an epigenetic tweaking ).  That chromosome filters out other pulses of conflicting messenger RNA  (from typical gene transcriptions going on) that might otherwise cause other cascades leading to oscillation in the pathway of mitochondrial energy production.

With one predominant nutrient  the dynamic is inclined toward working on a gradient; it is based on a dose response (ie: gradient of how much nutrient is put into equation)  and not just positive feedback (ie:  not just  "x" induces "y" and "y" loops through "z" to  make the action of "x" worthwhile enough  to keep doing things that way ), because  concentrations of a nutrient fine tunes the feedback response.  Biologists now call this  "hysteresis";  when a nutrient  modifies the traditional  stimulus-response relationship according to the history of past usage, and then the stimulus-response sets a high threshold (on a chromosome) for switching OFF in order to achieve a self-sustaining steady state burning the "favored" fuel.

I have followed my own research since 2007. I started, via Dr Barry Peatfield, with Dr Broda Barnes (thyroid) and then Dr William McK Jeffries (adrenal).  Then, I found Carole Baggerly at GrassrootsHealth and Dr John Cannell at Vitamin D Council.  later still, I found Michael Pollan, Gary Taubes, Dr Mercola, Dr Kurt Harris, Dr Robert Lustig  and the wonderful Jimmy Moore with his podcast back library.  I also found Dr William Davis and this excellent blog.  

What makes Dr William Davis special is that he does not promote just one thing (i.e. vitamin D3); instead he integrates the latest knowledge and provides guidance for a healthy lifestyle (for heart patients) covering lipids, blood sugar control, thyroid (iodine, T4, T3) and adrenal hormones (DHEA), vitamins D3, K2 and niacin, fish oil, carbohydrate restriction and grain elimination.  Whats more, as a practicing cardiologist, we get the considerable benefit of feedback from his ongoing patients.  

I am pleased that the blog is concise and that it is not behind a paywall.  There are plenty of blogs which delve into every detail of every study, but thankfully this is not one of them.

So, thanks to you Dr Davis.

@Might-o'chondria-AL

Satiety seems to be the key factor for adherence. Like some say, hunger is not an option long term.

Fuel partitioning is the distribution of fat between fat cells and all other cells, i.e. storage or consumption. Nutritional status would depend on this. If too much fat is shunted toward fat cells, then all other cells don't have enough and call for more. Fat cells themselves can call for more in spite of being full through their own hormonal signals. Insulin is the primary determinant for fuel partitioning. It's also the determinant of which fuel to burn.

Incidentally, I thought that cells could switch on and off at will which fuel they burnt in their mitochondria. Since insulin is the primary determinant, and since cells can turn on and off insulin receptors, they can control their own choice of fuel. For example, if a cell contains its quota of glucose, it will turn off insulin receptors to prevent any more glucose from entering the cell. As it does so, it also causes a change in the signaling that would otherwise tell the cell to burn glucose, i.e. insulin. So while it is insulin sensitive, it burns glucose. But as soon as it's insulin resistant, it stops burning glucose and starts burning fat instead. This is normal insulin resistance, not pathological. But pathological insulin resistance applies to Dr Davis' post. Carbs cause this at some threshold.

@Martin:  I think you'll find Paul's article I linked to above (now published) rather interesting.

Martin Levac - do NOT expect miss sane to understand what you wrote - her mind is made up, and if anyone does not agree with her, they are wrong, wrong, WRONG, and  simply making assertions - as she endlessly asserts.

Hi Martin Levac and anyone still reading,
Thanx for the fuel partitioning orientation.   Maybe this elaboration will add to  your perceptions of fuel burning.

Lipids (a.k.a. fats, fatty acids) actively induce the metabolic mechanism to preferentially burn themselves ( technically speaking for researchers : dietary fat gene transcription factor PPAR downstream induces  the pyruvate dehuydrogenase kinase 4,  PDK-4; which then reduces the levels of the enzyme pyruvate dehydrogenase and thus restrict glucose burning).

Conversely, glucose triggers the mechanism to preferentially burn itself and by gene transcription stops lipid (fat)  burning (technically speaking for researchers:  insulin/glucose keep cell full of malonyl-CoA and this inhibits enzyme carnitine palmitoyl transferase, CPT;  fat can not get  shunted into the mitochondria fro burning). "Hysteresis"  ( explained previously and admittedly poorly)  is how there is chromosome threshold set up for controlling switching to burning one fuel vs. a different fuel;  potential to burn multiple fuels is not the same as getting to chose which fuel to burn.

Insulin, and not just glucose, boosts glucose burning (glycolysis) and stymies fat burning (lipolysis); yet not all tissue groups have the same insulin sensitiviy. This is additionally relevant,  since say +/-  half of glucose is used by us without any involvement of insulin.

Age is worth some precise discussion, especially since Type II diabetes is sometimes likened to advanced metabolic aging. With age the use of glucose for burning as energy increases, relative to the burning of fat & protein. This is notable in the heart, liver and brain;  while in the muscles the burning of glucose does relatively decrease compared to one's youth, but the burning of fat & protein decreases proportionately even more so.  In other words, post-prandial glucose favors burning glucose and due to hysteresis the mitochondria stay keyed to burn glucose;  even after the glucose levels drop back down to the pre-meal glucose level.

Again, age and genetic obesity,  engender a decrease in leptin hormone response  (technically speaking for researchers: there is less hypothalmic alpha melanocyte stimulating hormone being made by  POMC,  pro-oipo-melanocortin). The increased glucose burning  generates more age related metabolic problems, such as obesity;  and  so, what we did in our youth is not always what we can  do  with impunity.

When diet  relatively limits carbohydrates this  sets  the "hysteresis" threshold for mostly burning lipids (&/or protein) in the mitochondrial complex II;  this, however, does not mean glucose is not used as some fuel somewhere.  When blood glucose is low the atoms of Carbon from glucose burned  aren't burned in the mitochondrial complex I (technically:  don't make NADH from glycolysis); but rather, that glucose Carbon is put into the Pentose Pathway (technically:  makes NADPH ).

Age is notorious for oxidative stress  (oxygen radicals on the loose in cells) and having low glutathione  (key anti-oxidant our cells make); glutathione, for it's part get's it's oxidant reducing power from the pentose pathway's NADPH.  Age commonly expresses less of the enzymes  that drive the production of  glutathione  (researchers:  age depletes isocitrate de-hydrogenase, the enzyme  needed for mitochondria to make NADPH  via NAP-   which interacts with glucose-6-phosphate dehydrogenase, the  rate limiting enzyme needing to be upregulated to keep the pentose pathway going).  

In other words, age reduces our alternate pathway of glucose burning  and we get more oxidative stress  from using mitochondria complex I  for glycolysis;  mitochondria complex I burning for energy naturally spins off more  amounts of reactive oxygen molecules, these  can go on to potentially damage a cell.  A relevant example is that the shuttling of NAD+ to NADH from glucose burning in the mitochondria complex I has a potential oxidative  impact on the pancreatic Beta cells reaction over time;  youth and genetic fortune can keep cellular glutathione levels high to counter-act this Beta cell oxidative stress.

Low blood sugar, like hypo-glycemia,  upregulates  some cell's  gene activator of GLUT 1  (glucose transporters in a cell);  this indicates the carbon atoms from glucose are not being burned in mitochondrial complex I (ie: not doing glycolysis),  but rather the pentose pathway is burning the sparse glucose.  At this point a high enough threshold has been reached to switch OFF mitochondial complex I glycolysis and the body is switching ON to use mitochondrial complex II for getting  energy by burning  fat (researchers: Beta-oxidation has prepped lipid carbon atoms to burn ) .

@Might-o'chondri-AL

Thanks for the explanation. But I must admit that I will probably forget most of it pretty soon. I prefer to stick to simpler concepts. For example, heavy exercise depletes glycogen, which must be replenished. Cells open up more insulin receptors for this, they become insulin sensitive. If we don't eat carbs, this is done only as fast as the liver can put out glucose. If we eat carbs it's done as quickly as the carbs we eat. Considering that we can't store much more than about 2,000kcals of glycogen, mostly in the liver anyway, this is done _very_ quickly, a few minutes at most probably. As soon as that's done, cells close down their insulin receptors, they become insulin resistant. I'm just explaining what I understand, not necessarily how it really works. Anyway, as Taubes said, this effect lasts 36 hours at best, less if we eat carbs. So we could use this to prevent weight gain, but only if we don't eat carbs or not that much.

The weight gain can be explained by the shunting of glucose toward fat cells because all other cells are now insulin resistant since they are now replete with glycogen. Even if we believe that all cells will start using glucose for fuel instead of fat when we eat carbs, we still have to explain how the insulin receptors will be opened up when the cells are already replete with glycogen, and don't want to take in any more glucose. So basically, when we eat carbs all the time, we're not dealing with the choice of glucose/fatty acids in all cells, but only in fat cells. Because only fat cells now accept glucose. Then we end up with the associated problems Dr Davis talked about like higher estrogen and prolactin to name a few.

Does that fit in with what you know?

Erectile dysfunction relation carbs,  a re-constructed lost comment ....

Burning carbs (glycolysis)  for energy in the mitochondrial complex I  incurs super-oxide anions ( O2-) as  NADH generated .   Age  sees these super-oxides  anion levels increase and this can add &/or provoke pathological damage to the endothelial  vascular bed (for researchers: super-oxide locks up nitric oxide in the form of per-oxy-nitride); O2- + NO = ONOO-).

Once endothelial dysfunction is going on the extra cellular anti-oxidant SOD (super oxide dismutase) is decreased and this compounds the situation;  little super-oxide (O2-) gets scavenged and nitric oxide (NO) gets degraded even more. NO is the main signal gas for penile erection;  NO is a downstream vasodilator allowing the extra 50 - 90 mmHg blood pressure to get into the penis.

NO (nitric oxide  and nitric oxide  synthesase , NOS) works through a heme iron protein in hemoglobin  (researchers: via enzyme  heme oxygenase, due to NO affinity for FeII-heme protein) to act downstream on another enzyme (researchers: guanylate cyclase) to induce  a "second messenger"  inside the blood vessel's smooth muscle cells to relax and open. The "second messenger"  downstream from NO is the same molecule (researchers:  cyclic guanosine mono-phosphate, cGMP) targeted by Viagra; the drug works by stopping that "second messenger" from  degrading and thus vaso-dilation sustains erection.

In the male genital endothelium there are the  heme enzymes for NO to work through;  although with progression of  endothelial dysfunction  the NO is  less free, and more so if  always burning glucose in the mitochondrial complex I and spinning off oxygen radical (super-oxide, O2-) to tie up the NO  .  The erection's  status  is complicated by the fact that the "second messenger" (cGMP) that works to relax/vaso-dilate blood down there
is subject to degradation by another enzyme (researchers: phopho-di-esterase 5, PDE).

There is yet another key enzyme (researchers: soluble guanylyl cyclase,  sGC) that is part of the cascade leading from NO to the "second messenger" (cGMP) that normally keeps the levels of the "second messenger" (cGMP) degrading enzyme (PDE-5) from getting too high. Of course, with endothelial dysfunction and less NO involved in the erectile
cascade  there is less potential  ( less sGC)  to keep degradation enzyme (PDE-5) from knocking out the vaso-dilation;  then calcium rises inside the  blood vessel's smooth muscle cells,  less blood flows in and instead starts to flow out.

There is a parallel/back-up signalling gas produced in the endothelium for signalling; this is CO gas, it has a feedback  loop with NO gas and can entrain a cascade that also, downstream, produces the "second messenger" (cGMP) for vaso-dilation induced erection.  The draw back is , that,  CO has 1,500 times less affinity than NO for the early step of  connecting  with  iron heme in our hemoglobin; and, not only that ,  but CO will move off of the heme slower than NO would.

Using CO to drive the cascade  leading to downstream vaso-dilation  is  essentially  just plain slow in real time; and then too,  not enough of the intermediate enzyme (sGC)  that prevents degradation enzyme (PDE-5) is being made fast enough .  An  initial erection can be achieved in many instances through the agencies of CO &/or through a sequence of a little NO passing job on to CO;  unfortunately this erection fades and then can not be regained in a timely manner.

@Mito:  A loss of hepatic fat in a very short term carb restriction is a bit of a stretch to imply the reverse that carbs cause the fat accumulation per se.   There's also the problem with conflating hepatic fat with visceral fat.  Even all visceral fat doesn't appear to be the same - e.g. omental vs. retroperitoneal.

Oops hit post while a part of reply was highlighted so it got truncated.  Sorry so abrupt.  I believe this "reverse logic" is rampant and unfortunately used all too often to support certain contentions.  For example just because many lose weight cutting carbs doesn't make carbs fattening.  

I also added to that last sentence:  So many studies further confuse the subject because some show it's visceral, some subQ abdominal, some both, some none wrt various metabolic factors.

@Carb Sane

Yes, this "reverse logic" is rampant. But we call it "implication". Like so "this evidence implies that conclusion". Science is full of such "reverse logic". And, it's proof that scientists use their brains to figure out how things work. It also helps scientists devise tests to refute those implied conclusions. That's also how science works.

Incidentally, for the subject we're discussing here, there is _direct_ evidence that carbs cause excess fat accumulation. No need to refer to the previous evidence, or the previous implications, or the previous conclusions. In fact, there's about 150 years of it.

Now you're attempting to bring confusion yourself by pointing out how different fat tissue respond differently. We already know about that. It does not refute anything Dr Davis said about carbs. Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned.

Hi CarbSane,
Read me clearly:  I don't write that a carb automatically  always causes an iota of body fat;  and  I don't give a pass to dietary fat.    Doc, unlike me, has  a clinical practice to base his declarations on;  I am merely trying to understand any science that might validate his point(s).

Denmark " Inter99 Study"  of 3,164 adults with normal glucose tolerance tracked over 5 years data is interpreted in journal "Diabetic Medicine",, April 2009, vol. 26, issue 4, pg. 377-383.  Synopsis is:  2 hour post glucose (2hrPG; using oral glucose tolerance test as the glucose load) has  a relationship to overall degree of obesity; whereas fasting blood sugar has more of a relationship to larger abdominal/waist circumference.    

Doc's contention is carbs can raise the blood glucose and this contributes to getting fat;  which (2hrPG) the Inter99 study links to % obesity.   One  can argue  the issue from another direction;  namely that incipient obese fat, from any number of assorted causes  (ie: not carb induced) can , down the line,  cause the situation whereby 2hrPG ( blood sugar response) then goes on to predict waist circumference and BMI.

Omental adipose tissue is  considered as part of the  regulatory loop  of insulin sensitivity.  One of the causes of lipids (fatty acids, fats) going into the omental adipose cells (and liver cells) is when sub-cutaneous fat can't hold all the lipids presented to it (sub-cutaneous fat).

Size matters too, since large adipocytes produce more pro-inflammatory cytokines;  thus,  an individual with  factors  limiting pre-adipocytes from differentiating into functional adipocytes  is at risk of pumping up their  existing adipocytes.  This  is one way dietary excess  is modified by the metabolic coping  of each individual;  in other words not every obese person  is going to get Type II diabetes.

Omental macrophages, and their cytokines, are associated with greater liver inflammation; and an altered pattern of  fibrosis in the liver.  The omental macrophage risk to the liver exists even if there is no insulin resistance;  ie:   not only Type II diabetics but the obese  can have  liver risks.

Real men avoid grains (lectins, gluten, anti-nutrients), that's for sure. But that does not mean that they have to avoid all carbohydrates. Especially starches and glucose are, when cosumed in correspondence with your lifestyle, tolerated perfectly by the human body. It's time to get more specific doctor Davis. We cannot just keep advocating GCBC. VBR Hans

Martin, Dr. Davis made the specific assertion that carbs cause visceral fat accumulation (implied to a greater degree than fats or protein).  Where's the evidence for that?  Eating leads to fatty acids moving into fat cells and getting deposited.  That's not "fat accumulation" though.  Accumulation involves net deposition vs. mobilization and that is determined by how much carb, fat and protein someone consumes.   The statement "Carbs still cause excess fat accumulation, and all the other nasty stuff he mentioned." is unsubstantiated.  It is repeated over and over in the low carb echo chamber, but there's no evidence for it.

What has happened?!?  This comment section is ridiculous!  You trolls need your own site or forum to go nuts on and bash Dr. Davis there.  Or better yet, meet each other somewhere, throw your weight around in person, and claim your position as the smartest person in the world.

Hi Dr. Davis,

what is happening? No new post lately. On vacation? Sick? Tired?
I miss your musings and posts!
Cheers,
Renfrew

All - I think we should periodically go back to how our particular bodies evolved ..... (e.g Why/How do bears get fat before the winter).  Single season - meaning only available once per year - items are typically high in Carbs... Berries, Fruits, Roots, etc... Green leafy veggies are low in carbs... Grains from grasses are once per year.... highly processes they are acres of starch to our army of enzimes and produce huge insulin response... even Bears never had the availablity of wheat flour... otherwise they would have gotten fat enough, soon enough without having to go up and down all those mountain slopes looking for huckleberries and ants....

Man ... as usual ... is very efficient at what he does.....

You're an idiot and a charlatan.

Because on that list potatoes are pretty much the only thing listed that is actually bad and you probably burn more calories than you take in.