15 replies to this topic

[lucid]

Hey guys (and ladies!),
I'm a 28 yo male.
Weight: 235
BodyFat%: 12%

IGF-1: 231 ng/ml
Insulin (Fasting): 7.6 uIU/ml

Having bad cholesterol, I decided to switch to a very low-carb diet. I was <50g carb/day and was deep in ketosis for about 4 months. Big changes happened. Triglycerides went from 300-400 down to 80-95 (-70%). HDL went from 26->40 (+55%). LDL+VLDL went from 136 -> 130 (-4%). Lipid profiles (so far as I can tell), don't change that rapidly so I expect the results to improve over the next year.

For the first time in my life, I have blood work that indicates I'm not at risk for diabetes or heart disease. In the "before" era, I was in OK shape (16% bf). I didnt drink sodas, eat dessert or candy etc. I ate normal 'balanced' meals that included rice, whole grain etc.. So I maybe I just had bad genetics, maybe thats why my bloodwork sucked. WELL, nurture > nature.

Now there are some downsides to being in ketosis:
1. Fatigue: You muscles lose all their glycogen stores and replace them with triacylglycerol - triacylglycerol isn't as oxygen efficient in its metabolism. This means that you can't excercise close to your aerobic threshhold for very long at all.
2. Insulin Resistence: When you first start going into ketosis, your fasting blood glucose is AMAZING. My fasting glucose went into the high seventies. However, prolonged ketosis causes insulin resistence & increased fasting blood glucose. By 4 months in my blood glucose was mid/high nineties. This isn't normal insulin resistence -> it exists to route all existing glucose to the brain instead of the muscles and is reversed once you start consuming carbs (oddly enough).

For these reasons, I have stopped trying to be in ketosis and instead am doing just a low carb diet. Still no grains, no sugar (except that found in fruit), and few starchy veggies. What's the difference you might ask? Well I have added things like beans and fruit back into my diet. I'll post results in a month or two and we will see how that impacts the above results.

As I was reading up on ketosis and its effects. I found that the ketogenic diet was invented a long time ago (100 years) to treat epilepsy. The reason that it helps with epilepsy is that the brain starts consuming ketone bodies instead of glucose when in ketosis. This prevents seizures! So as a result lots of epileptic children were put on ketogenic diets. And... they found that when kids were put on ketogenic diets their height and weight velocity (increase / year) was very significantly slowed. This will start sounding very familiar to you dwarf mice fans -- Now guess what was happening...? Their IGF-1 levels dropped significantly from being in ketosis and it became evident that their growth was stunted. (Can provided references)

Ketosis causes IGF-1 to drop because a ketogenic diet isn't just a low carb diet, its a HIGH FAT DIET! Don't think 'Atkins' where you are eating steak and veggies. You have to control you protien intake as well (though it should be up a little bit). In a ketogenic diet, 75+% of your calories are going to come from fat! It might be starting to dawn on you how ludicous it felt: I was eating cheesy eggs & bacon to improve my risk for heart disease!!!! The reason that I mention that the ketogenic diet is really a high fat diet is because fat is the only macro-nutrient that doesn't stimulate insulin. Carbs stimulate insulin and to a lesser exent protien does as well. The picture should be pretty clear at this point how ketosis should impact IGF-1: High fat, medium protien and low carbs should radically lower the IGF-1 levels. And (as I'm hoping this audience already knows), IGF-1 levels dramatically effect aging in almost every animal its been studied in!

Now on to my question!!!
So I (kind of) screwed up. I didn't get a 'before' IGF-1 test. If you are going to do the same protocol, do this one thing. Get a complete 'before' test before you start - I was too axious to start, and boy I wish I had gotten it done. So here is my predicament:

I don't have a baseline for my before 'IGF-1', now as a secondary problem I went out of ketosis and switched to just being low-carb about a 3 days before my blood work.... I know, I know. Ughhhh. To make matters worse, the baseline for IGF-1 is very ambiguous and every single source that I have read has a different reference interval for IGF-1 for my age group. Some show its sex dependent some show its not. So are my IGF-1 and/or insulin levels low?

Anyways, thanks for reading. Please post if you found this interesting, would like to know more or think you can help answer my questions!!!

[Chupo]

Did your test show how much free IGF-1 you have or does it only show the total? Some of that could be tied up in IGF-1 binding protein.

Edited by Chupo, 08 July 2013 - 06:14 PM.

[Pour_la_Science]

235 lbs (106 kg) for 12% of fat Are you a body builder?

[lucid]

235 lbs (106 kg) for 12% of fat Are you a body builder?

Well, I've been strength training 4x/week for the past few years, so I'm strong. But I'm also 6'4" so I'm not that thick - more like tall and muscled. I'm trying to get down to 9% so my abs will show better

Did your test show how much free IGF-1 you have or does it only show the total? Some of that could be tied up in IGF-1 binding protein.

The test didn't specify. I assume its free... It would probably be hard to measure if bound. I'll ask my Dr when i review the results with him this week, so thanks for asking!
What would knowing that change? Do you have seperate ranges for both?

[Pour_la_Science]

Did your test show how much free IGF-1 you have or does it only show the total? Some of that could be tied up in IGF-1 binding protein.

I second that. According to that review (http://biomedgeronto.../67A/6/626.full ), 99% of IGF-1 is bound !
Moreover, according to that, at the beginning, the labs were testing only the total form (must be easier to do that) so I bet if it's not specifically written free IGF-1, this test is pretty useless :

Some cross-sectional and prospective studies (37–43) suggest a positive association between IGF-1 (and in some cases IGFBP-3) and atherosclerosis. Others (44–54) found that low IGF-1 is a predictor of ischemic heart disease and mortality, consistent with the potential antiapoptotic, antioxidant, and plaque stabilization actions of IGF-1. Several large prospective cohort studies failed to systematically confirm these findings (55–60). Several methodological constraints can explain this variance. So far, most studies have used total extractable IGF-1 as an estimate for IGF-1 activity in vivo. However, this provides only a crude estimate of the active hormone, as less than 1% is in its free form, and only free IGF-1 is believed to readily cross the endothelium and interact with its receptor. Of note, IGFBPs, in addition to their potential IGF-1 independent actions, might modulate IGF-1 bioactivity without any changes in the extractable concentrations of total IGF-1.

Edited by Pour_la_Science, 09 July 2013 - 01:41 PM.

[mikeinnaples]

In the "before" era, I was in OK shape (16% bf). I didnt drink sodas, eat dessert or candy etc. I ate normal 'balanced' meals that included rice, whole grain etc.. So I maybe I just had bad genetics, maybe thats why my bloodwork sucked.

You don't think the whole grain and rice heavy diet was contributing to your problem?

[lucid]

In the "before" era, I was in OK shape (16% bf). I didnt drink sodas, eat dessert or candy etc. I ate normal 'balanced' meals that included rice, whole grain etc.. So I maybe I just had bad genetics, maybe thats why my bloodwork sucked.

You don't think the whole grain and rice heavy diet was contributing to your problem?

Well it wasn't rice heavy, but I guess that those must have been contributing since eliminating them has really improved my lipid profile

[lucid]

Finally setup the review with the Doc today - He didn't know the whether the test was free or total IGF-1 :/ Bummer. He also didn't know how fast IGF-1 levels changed. So I don't know whether going out of ketosis for a few days prior to testing effected my IGF-1 levels much.

He gave me a pretty glowing review though -- I really didn't make some pretty dramatic changes to my blood work over the past year and a half.

[madanthony]

Well, here are MY comments. I do not believe a low carb diet is good for you AT ALL. I believe people see results on them vs. not because of the KIND of over-processed nutrient poor carbs they were eating. If you want to improve your cholesterol the HEALTHY way, you need to look to your hormone levels. If any of your hormones is low, such as your thyroid (and by low I mean TSH>1.9, then your body will make cholesterol since it is the substrate from which your hormones are made. So what is your TSH, FREE T4, FREE T3? If they are not what they should be, consider what deficiencies you might have: zinc, iodine, selenium, tyrosine, methylB12, copper. (Perhaps others). Also think about whether you might have trouble absorbing any of these (I take zinc picolinate, other forms are very poorly absorbed). Think kabout whether or not you might have higher needs for some of these than others (I have a higher need for zinc...I rip through it like gangbusters when I have allergies to the point that my thyroid goes out if I do not aggressively supplement). For info on the link between thyroid and cholesterol, look here: http://www.lef.org/m...t_blood_02.html . There are other supplements that lower cholesterol significantly like pantethene, which is B5, a supplement according to acu cell lab that is undersupplied. I believe in selecting supplements one should make sure to cover the bases of those necessary for life first before exploring odd plants and such. So see if your thyroid is right first then B5 levels. Acu cell showed a representative plot of blood levels of B vitamins in people taking those B100 and B50 pills and it showed a sharp dip in B5 levels.

[galtsgulch]

Well, here are MY comments. I do not believe a low carb diet is good for you AT ALL.

As noted in Wikipedia, "[t]he ketogenic diet is a mainstream, nonpharmacologic therapy that was developed to reproduce the success and remove the limitations of the non-mainstream use of fasting to treat epilepsy." There have been several studies (copies attached) that propose neuroprotective and mitochondrial benefits from Ketogenic diets, and favorably compare the health results with Calorie Restriction.

Attached Files

•  Neuroprotective and disease-modifying effects of the ketogenic diet (2006).pdf   105.92KB   6 downloads
•  The Neuroprotective Properties of Calorie Restriction, the Ketogenic Diet, and Ketone Bodies (2008).pdf   433.09KB   8 downloads

[madanthony]

Well, neither my father nor I could survive on a low carb diet. I was getting 3 low blood sugar attacks a day. All I had to do is walk from one bulding to the next at work and I'd get low blood sugar shakes and sweats. I am not diabetic but my father is/was. Dr. Julia Whittaker quotes the 1927 studies on carbs and diabetes in his book and he trains diabetics at his clinic in California to overcome diabetes with complex carbs. I know for a fact he's right because I avoided the genetic diabetes in my family with this knowledge. HOWEVER, I'm not interested in debating that. I am really interested in how to maintain glycogen stores over a marathon cycle ride. Anyone? (Odd. It is about 9:30 pm but it says I posted in the wee hours of the am???)

Edited by madanthony, 11 August 2013 - 01:47 AM.

[misterE]

Low levels of IGF-1 are found in type-2 diabetics and people with insulin-resistance. Insulin stimulates IGF-1 production, if you are insulin-resistant thou, this doesn't happen and IGF-1 levels decline. As IGF-1 declines, the cells in the body undergo apoptosis (which could be either good or bad depending on the context).



It has long been known that ketogenic-diets induce insulin-resistance by reducing secretion of insulin from the pancreas and increasing the rate of lipolysis, gluconeogenesis and proteolysis (thus increasing the blood concentration of free-fatty-acids, glucose and branched-chain-amino-acids, all of which are elevated in diabetics).



This type of diet (ketogenic) along with prolonged fasting also promotes insulin-resistance by increasing the accumulation of FFA’s and triglycerides in organs like the skeletal-muscle, pancreas, heart, kidneys and liver --after all, these organs have to eat too and if you restrict carbohydrates the organs accumulate fat in order to survive. When you begin eating carbohydrates and spiking your insulin again, the fat migrates out of these organs and back into the adipose-tissue (storage) which allows the organs to become lean (and insulin-sensitive) again [1-3] … it’s a double edge sword in a way, but my belief is that it is best to keep lipolysis inhibited and very important to spike your insulin (by eating more starchy foods) on a daily basis. Keeping fat intake low when eating starches prevents any further fat-gain, albeit the insulin produced in response from the starch will slow fat-loss.





Hope this helps.



[1] Diabetologia. 2005 Oct;48(10):2097-107. Inhibition of adipose tissue lipolysis increases intramuscular lipid use in type 2 diabetic patients. van Loon LJ, Manders RJ, Koopman R.

[2] Am J Physiol Endocrinol Metab. 2005 Sep;289(3):E482-93. Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans. van Loon LJ, Thomason-Hughes M, Constantin-Teodosiu D.



[3] Int J Clin Pract Suppl. 2004 Oct;(143):9-21. Dysfunctional fat cells, lipotoxicity and type 2 diabetes. DeFronzo RA.

Edited by misterE, 19 September 2013 - 03:14 AM.

[misterE]

Anyone?

You are absolutely right. The classic study which told us what caused diabetes was conducted by Dr. Shirley Sweeney in 1927 where he took a group of college students and separated them into four groups. One group was put on a high-carbohydrate diet (50% starch/50% sugar), another group was placed on a high-protein diet (lean-meat, egg-whites and lean-fish), another group was put on a high-fat or ketogenic-diet (mayonnaises, egg-yolks, butter, olive-oil), the last group was told to fast (not to eat anything).

What Sweeney discovered was that all the groups were diabetic except the high-carbohydrate group. Which I explain exactly how that happened here.

Another huge clue was that during WWII. The Nazis would confiscate the livestock of the occupied countries in order to feed their troops animal-products, the citizens of these occupied countries could no longer eat (much) meat, dairy and eggs and had to start eating grains and vegetables, as a result the death from diabetes and heart-disease in Europe during WWII declined dramatically (after adjusting for war mortality of course)… only to return after wartime, along with the animal-fats.

Studies from the Pritikin Longevity Center have shown numerous times to completely reverse metabolic-syndrome in nearly 3 weeks by using a high complex-carbohydrate (starch) diet. Dean Ornish and Caldwell Esselstyn have shown actual reversal of atherosclerosis using a high-fiber complex-carbohydrate diet.

Edited by misterE, 19 September 2013 - 03:50 AM.

[NeuroGeneration]

Hey guys - I know this thread is a bit dated, but if you're still active, I'm facing a real-world issue related to blood sugar control & carbs. Any help / thoughts would be appreciated. I posted here: http://www.longecity...arb-keto-diets/

[Brett Black]

And (as I'm hoping this audience already knows), IGF-1 levels dramatically effect aging in almost every animal its been studied in!

Maybe not in humans though. Laron syndrome features lifelong congenital low IGF-1 and doesn't appear to have any dramatic effect on lifespan. It does result in obesity, dwarfism, weak bones and other problems though, and IGF-1 generally appears to be associated with heart, muscle, skeletal and brain protective and maintenance effects. It may be of importance that rodent IGF-1 is high throughout life whereas human IGF-1 levels continuously decline after puberty.

[Cris Barrows]

Well, neither my father nor I could survive on a low carb diet. 

 

That suggests a genetic connection. Do you know your APOE gene type. If you have an E4 then your ability to process FATs will likely be a major problem and you will struggle on HFLC. 

 

If you are normal weight or below and eat a lot of carbs then that might indicate you have many copies of the AMY1 gene. Copies go from 1 to 15. The number indicates the amount of amylase in your saliva - essential for efficient starch processing. Those with a low value have real trouble with starch and tend to become obese easily and for them HFLC is the best option.

 

The genetics for different groups have changed over time most likely due to adaption in different geographical areas. Tropics may have favored more carbs - ease of access to fruits etc. Whereas more northerly climes would favor hunter styles and a greater dependence on animal food and fats. 

 

The point is that it is not reasonable to recommend a one diet type fits all people, or that one type is unhealthy for one so must be unhealthy for everyone. And while HFLC doesn't work for you, it certainly works extremely well for many people, and probably a high percentage judging by the current obesity and diabetes epidemics.