Figure 2. Cox proportional hazards survival curves demonstrating
time to acute MI for patients with a yearly calcium volume
score change > 15% or < 15%. Callister et al, 2004 ATVB.
time to acute MI for patients with a yearly calcium volume
score change > 15% or < 15%. Callister et al, 2004 ATVB.
TITLE: Progression of coronary artery calcium and risk of first myocardial infarction in patients receiving cholesterol-lowering therapy.
Free PDF click HERE. Raggi P, Callister TQ, Shaw LJ. Arterioscler Thromb Vasc Biol. 2004 Jul;24(7):1272-7.
OBJECTIVE: Statins reduce cardiovascular risk and slow progression of coronary artery calcium (CAC). We investigated whether CAC progression and low-density lipoprotein (LDL) reduction have a complementary prognostic impact.
METHODS AND RESULTS: We measured the change in CAC in 495 asymptomatic subjects submitted to sequential electron-beam tomography (EBT) scanning. Statins were started after the initial EBT scan. Myocardial infarction (MI) was recorded in 41 subjects during a follow-up of 3.2+/-0.7 years. Mean LDL level did not differ between groups (118+/-25 mg/dL versus 122+/-30 mg/dL, MI versus no MI). On average, MI subjects demonstrated a CAC change of 42%+/-23% yearly; event-free subjects showed a 17%+/-25% yearly change (P=0.0001). Relative risk of having an MI in the presence of CAC progression was 17.2-fold (95% CI: 4.1 to 71.2) higher than without CAC progression (P<0.0001). In a Cox proportional hazard model, the follow-up score (p=0.034) as well as a score change >15% per year (P<0.001) were independent predictors of time to MI.
CONCLUSIONS: Progression of CAC was significantly greater in patients receiving statins who had an MI compared with event-free subjects despite similar LDL control. Continued expansion of CAC may indicate failure of some patients to benefit from statin therapy and an increased risk of having cardiovascular events.
PMID: 15059806
Cardio Controversies: Dr. Callister MD
I think Callister is cool. First he found statins were associated with regressed EBCT scores in 1998 but then confessed up when he could not replicate it in several subsequent trials. He has even postulated why. Correctly I think!
He and his colleagues have found a dilemma in current cardiology concepts, much like Dr. Superko. Despite LDL < 120 mg/dl and treatment with statins, patients progressed to an MI when the calcium volume score via EBCT increased > 15% annualized. In fact, they summarize that "the relative risk of suffering a MI in the presence of CVS progression was 17.2-fold (95% CI4.1 to 71.2) higher than that of subjects without progression (P<0.0001)."
Our goal at TYP as designated by Dr. Davis from his extensive experience and research is for EBCT annualized progression of no more than 10% to halt all risk of long-term clinical CAD events. Naturally, some EBCT regression is desirable.
Is LDL Reduction Necessary?
For reduction in hard clinical events, is LDL reduction really necessary? Actually, I don't think so... From lipid researchers like Dr. Barry Sears PhD on omega-3 and the tremendous outcomes from the secondary prevention Lyon Heart Diet trial, we know that with a significant reduction of dietary omega-6 toxic vegetable oils and sufficient increments of dietary omega-3 (ALA, EPA, DHA), clinical CAD events can be nearly halted in very high risk group of CAD individuals. Moreover, with only minor improvements in the n-6:3 balance a reduction in all-cause mortality (cancer, suicides, accidents, etc) in addition to CAD mortality and events was observed in this landmark study. Recall, these improvements were witnessed with no improvements in total HDL (final 49 mg/dl) or LDL (final 161 mg/dl). I always have to ask why save the heart and coronary vessels yet advance to experience cancer and/or suicide and depression? One of the most tragic and saddest stories that I have come across related to the low-saturated fat debacle is that of the famous Dr. Pritikin who conquered heart disease but committed suicide after silently battling leukemia. What was he missing? Could his demise have been prevented?
Low Dietary Saturated Fat
Why may low saturated fat be dangerous for the long-term? Can a 'deficiency' in dietary saturated fat be as insiduous and quietly dangerous as cancer or subclinical atherosclerosis itself?
I see a lot of HDLs in the 20s 30s 40s (or HDL2b nonexistent to single-digit). What is wrong with these kind of numbers? For one, according to clinical trials, they are highly associated with CAC progression and early events. Of course, there are cases that are exceptions to the rule... for instance if you are . . .
(1) Nissen infusing HDL-apoAI-recombinant pieces into your arm every night (JUST KIDDING... don't get any stupid ideas)
(2) an apo A1-Milano carrier
(3) allergic to kryptonite *haa*
(4) consuming boatloads of niacin or omega-3 fish oil until gills grow
Are low HDLs a sign of dietary saturated fat deficiency? Or just high carbohydate intake? Or both? Moreno JA et al showed that with a high fat diet (40%) both high saturated fat (20% SFA) and high monounsaturated fat (22% MUFA), shifted individuals equally from pattern B to A when compared to a high carbohydrate (CHO 57%) diet (J Nutr. 2004 Oct;134(10):2517-22). PDF click HERE. However, like other saturated fat studies, only the SFA diet across every apo E type (4/3, 3/3, 3/2) raised the HDL to the highest degree. Interestingly, apo-AI was increased as well to the greatest magnitude with the high saturated fat diet and was the case for every apo E genotype. Both HDL and apo-AI are atheroprotective and associated with plaque regression. See below chart (p<0.05). FYI, these diets in healthy volunteers were still very VERY high carbohydrate at (yikes) 47% and explains why a higher majority of individuals were pattern B (predominance of small dense atherogenic LDL) to begin with, particularly in the males. Certainly, I know I would immediately be clinically T2DM with this type of diet.
Callister's Other Findings: 'Incomplete Effectiveness of Statins'
Callister et al concluded that 'statin resistance' may be responsible for the lack of efficacy for these drugs in preventing hard clinical events observed in this trial. How about...
Lack of HDLs?
Excessive carbohydrates? 47+% Carbohydrates in the AHA 'low fat' diet?
Lack of dietary saturated fatty acids?
The authors concluded that "molecular mechanisms—as yet not fully understood—could help explain the incomplete effectiveness of statins therapy. The HMG-CoA reductase enzyme is a pivotal rate-limiting enzyme in the production of intracellular cholesterol and is selectively inhibited by statins. To inhibit excess synthesis of cholesterol, the HMG-CoA reductase enzyme is degraded in the presence of high levels of intracellular mevalonate and sterols. Statin resistance at the cellular level has been described to occur via 2 mechanisms: overexpression of the gene regulating secretion of the HMGCoA reductase enzyme and loss of degrading ability of the enzyme in cell cultures exposed to high concentration of lipoproteins and lovastatin in the medium."
OK... well they were close. HMGCoA reductase is certainly controlled by several factors. Ness and Chamber discuss this 'cholesterol buffering capacity' effect of HMGCoA reductase, the enzyme that produces LDL-Cholesterol (the good lbLDL and the 'bad' sdLDL) and is mechanistically inhibited by statins. Unfortunately like all interconnected systems in biological environments, feedback control ultimately inhibits or stimulates HMGCoA reductase activity based on many factors which are regulated by needs for growth, reproduction, fasting v. fat-storage, and relaxation. Click HERE.
--dietary cholesterol downregulates (yup... cheap-egg-yolks vs. Crestor; yolks WIN)
--hyperinsulinemia turns it on (poor glycemic diabetic control, high-carbs-low-fat-idiocy, again)
--hypothyroidism turns on
--peri- and menopause (low estrogen states -- or like those induced by $*%&@# contraceptives and $*%&^! progestins)
--high cortisol (mental stress, physical stress)
--lack of bile salts (taurine deficiency)
Factors NOT Affected by Statins: Lp(a), IDL, Small LDL, Microbes
Callister and the other authors are brilliant! In addition, they concluded: "Because we did not measure hemoglobin-A1c, we were unable to verify whether the glycemic control had an effect on CVS progression and development of MI. Lipoproteins not affected—or incompletely affected by therapy with statins—such as Lp(a), small dense LDL, and other mediators of vascular damage (viruses, homocysteine, fibrinogen, Chlamydia Pneumoniae, and others) may also have played an important role that could not have been detected because of the design of our study."
What Does Lower Lp(a), IDL, Small Dense LDL and Microbial Burden?
Oh please... Gentle Readers... I hope you get this correct.
Yes?
Saturated fatty acids, my dear audience members, of course.
Synergistically with a low LOW carbohydrate diet (or no carb).
Did you know that coconut oil, grassfed ghee/butter, cream, tallow, lard (which contain short-, medium- and long-chained saturated fatty acids) control and kill yeast, parasites and other microbes like Giardia, Salmonella and Campylobacter, in vivo and in vitro?
Krauss is in the House! The Three Axes of Evil
Yes -- of course (without Superko's help) Krauss has figured it out again and confirm the theories above as well as what we already acknowledge and tackle at TrackYourPlaque. Subfraction of lipoproteins yields the 'death' bands on ion mobility analysis which are independent subsets of cardiovascular risk. (Krauss et al, Arterioscler Thromb Vasc Biol. 2009 Sep 3. Not free yet.)
(PC1) LDL-associated risk: Concentration-sdLDL, Small Dense LDL, VLDL [Lipoprotein (a)]
(PC2) Metabolic Syndrome/Hyperinsulinemia pattern of decreased large HDL, increased small/medium LDL, and increased triglycerides (eg, Pattern B)
(PC3) HDL-associated protection: large HDL subfraction ('absent' band)
Note: Krauss does not list Large LDL-P as one of the axes of coronary risk. After reviewing 3 large landmark trials, he and the other researchers concluded Large LDL are not associated independently with CAD risk. Again, the presence of small LDL-IVb (the densest of 7 subparticles) is associated with risk and progression of plaque, not a high particle count of Large LDL.
Krauss and the other authors state, "Our study demonstrated that (1) levels of small/medium LDL particles are associated with [CV disease] and (2) levels of large LDL particles are not significantly related to cardiovascular disease, is consistent with other large prospective cohort studies whose data were obtained by 2 different lipoprotein measurement techniques: the Quebec Cardiovascular Study (GGE) and the Multi-Ethnic Study of Atherosclerosis and Women's Health Study (NMR). (p. 5)"
Large-LDL are Not Associated with Increased CAD Risk
This bears redundancy. Many cardiologists and even NMR experts do not understand this concept. Repeat... Krauss and other cardiologists found no increased risk associated independently with the presence of Large LDL.
Why is Large LDL even implicated sometimes?
Are fire-fighters implicated in causing atrocious out-of-control fires?
No. That is frankly ridiculous...
The arsonist is the smallest densest LDL. (See PC1 or PC2.)
And, the co-conspirator is the lack of large HDL2. (See PC3 or PC2)
(Read: dietary saturated fat deficiency. Excessive compliance with the AHA low chol/sat fat indictment).
Genetically we are all different -- some individuals naturally produce more Large LDL (apo E4? these folks elude infectious agents better, esp coupled with Lp(a); unfortunately the CAD is concordantly worse on inappropriate diets, e.g. non-ketogenic). However, when the NMR is examined, these individuals who have both CAD and bunches of Large LDL exhibit the 'death' band. Subfraction particles of LDL-IVb will often be 10x higher than normal. Or even 20x higher. What's normal and optimal? Optimal is none to 0.60% in my opinion.
Pattern A + the tiny LDL-IVb 'death' band is not a good thing.
You only need one axis of 'evil' for heart disease and EBCT progression.
Paleo folks sometimes have very high LDL mass and stunningly enormous proportions of Large LDL. Funny... this is also observed in individuals in longevity and centenarian studies. The long-living 100-year old Ashkenazi Jewish (pro-bands) have enormous HDL and Large LDL yet the small dense LDL was minor consisting of ~6-7%. Is all that Large LDL harmful? I doubt it. Their offspring have HDLs like us mod-high fat Paleo folks of 80s-100s. Okinawan centenarians also have enormous HDL of 60s with consuming goat milk full of saturated fat (MCTs), lard, fatty pork and gamey goat sashimi. Their LDLs are high in the 100-120s mg/dl like the Ashkenazi.
Read here: Benefits of High-Saturated Fat Diets (Part II).
For the Paleo/Primal/PP folks, if the LDL is mostly (or all) large, no problem. If however there are some of the smallest densest stuff (subspecies: LDL-IVb, the black sheep) and no large HDL2, then... it... maybe a problem. LDL-IVb is eradicated within 4wks with the right diet. Low low carb, fat and protein, Paleo.
Only subfractionation of the lipoproteins will identify the culprit.
Statins Fail to Improve ALL 3 Principal Components (PC)
Do statins help with any other of the above independent axes of coronary risk: PC1, PC2, or PC3? Or other identified CAD risk factors: vitamin D deficiency? Omega-3 deficiency? Hypothyroidism? Excessive omega-6 clogging up cell membranes and raising serum insulin and inflammatory markers?
Well... statins raise vitamin D. (yeah... Sunshine/ supplement v. Crestor which raises vit D 159%? Sun+Vitamin D WIN. When my blood [25OHD] increased from 20 to 70 ng/ml (350%), my HDL increased 29%. OK... here is a vitamin D formula: every 10% vitamin D conc increase = 1% HDL increase; according to Castelli, every 1% HDL increase is equivalent to 2-3% CAD relative risk reduction)
Well...statins may raise HDL max 5-15% yet niacin raises HDL 30-200% (depending on duration and patient population).
So the action on promoting regression via HDL by Niacin is 2 to 40x more than statins.
Niacin prominently lowers Lp(a), small dense LDL/IDL, triglycerides and provokes shifts to Pattern A. In the HATS trial, recall, after 3 yrs, niacin raised HDL 30% and HDL2 60%. Niacin was associated also with reductions in blood pressure. Statins are not in any trial.
In fact, any non-synthetic, therapeutic intervention that raises HDLs also lowers Lp(a), IDL, small dense LDL/medium LDL and triglycerides. And increases nice large buoyant LDL. Indeed, these lipoprotein species all improve in parallel. Conversely, they are exacerbated in parallel. With no exception, any strategy that raises HDLs consequently affects blood pressures positively downstream (eg, carb restriction, body fat loss, lean muscle gain, yoga, omega-3, vitamin D, saturated fat intake, thyroid replenishment, hormone optimization, many antioxidants and proanthocyanidins).
Except statins. What the authors missed mentioning was that in addition to 'statin resistance', statins worsen Lp(a) and Percent-sdLDL. And they fail to shift to pattern A. What else?
Statins s*ck.
Correctly Catching the Calcification Culprit(s)
TrackYourPlaque is a self-management program. To optimize the program and control plaque, one must accurately and knowledgeably assess personal and familial risk factors that caused suboptimal lipoproteins and/or positive EBCT scores and progression. The three factors listed above comprise 99% of the most common coronary culprits.
If one is just trying to beat down the LDL-Particle Count into submission and fails to take into account the three 'axes' of coronary risk, one will invariably miss the big picture.
Is it... dangerous...??
Certainly... it is not equivalent to EBCT stabilization or regression. Targeting and ameliorating the correct coronary culprits on the other hand yields potent control on plaque and reduce EBCT calcification progression to < 10%. For regression in 9-18 months on EBCT, 'perfect' lipoproteins are not mandatory but a trend toward improvements in both reductions in small dense LDL, IDL, Lp(a) and increases in HDL2 and relative LDL-buoyancy are requirements. Control of hypertension, more vitality, loss of body fat are all extra side perks.
Do you have 'leaky gut' where microbes are flowing into the blood stream from the intestines?
Do you have low HDL?
Do you have high small-LDL?
Do you have Pattern B?
Do you have Lp(a) and/or high homocysteine?
Do you have progression or calcium score > 10% annualized?
Do you have premature CAD or stroke or peripheral vascular disease or renoarteriosclerosis in your family history?
Do you have proteinuria, dialysis or chronic kidney disease in your family?
Do you have heart failure in your family history?
Do you have 'statin resistance'?
Then... one cannot hesitate or prolong an approach that is more targeted and aggressive than the one that Callister and his colleagues discussed ('incomplete effectiveness') associated with a 17.2-fold MI-risk in 6-7 years.
Ketosis/niacin, low LOW carb Paleo diets, mod-high SFA diets, high omega-3 supplementation, dietary omega-6 elimination, hormone optimization, cardio/weights and many MANY other TrackYourPlaque strategies improve all three axes of high cardiovascular risk.
Related posts:
Egg Yolks and High SFA Diet Raise HDL2, Lower IDL VLDL triglycerides, and Increase LDL Particle Buoyancy
Benefits of High-Saturated Fat Diets (Part I): Krauss 18%-High SFA Diet Lowers sdLDL particularly LDL-IVb, Raises HDL2b and lowers IDL VLDL triglyerides
Benefits of High-Saturated Fat Diets (Part III): High SFA, Low Carb Paleo Diet annihilate sdLDL from 1000nmol/L to nearly no particles or 'None', Raises both HDL2/HDLs 200-400%, Lowers IDL VLDL triglyerides, Lowers Lp(a)
HDL2b: Quintessential Regression Particle and How to Raise It
Lp(a) and Women's Heart Risk
Umbellularia Californication: SFA kicks olive oil's *ss
Lp(a) and the Power of Fish Oil (8.5 grams/d EPA DHA)
38 comments:
Really enjoy your blog. I have a question for you about niacin. I had the spectracell NMR test done and it showed the following values in nmol/L
VLDL 33
LDL total 678
RLP 79
Dense LDL III 195
Dense LDL IV 82
HDL total 8425
Bouyant HDL 2b 1821
LPa was approx 3mg/dl
Most troubling to me was my description of LDL phenotype as pattern B at 20.02 nm. As I understand it from Davis's blog niacin would improve a number of these parameters but I worry about elevating Hba1c...after all, isn't keeping a1c low paramount? I'm 50, and my heart scan was a zero.
Thanks,
Drew
Dr B G,
It's one thing for me to use my simple logic and powers of deduction to make assumptions, but when someone of your status writes entries like this, it definitely soothes the mind knowing you feel the same way--very helpful, very thoughtful, and again I appreciate that you take the time to piece together all these facts and explain away. This particular entry hits close to home, regarding statins. I hate them.
Two reasons--my poor father (today's his birthday, by the way) was put on 80mgs Lipitor after his first CABG. He was also told to cut out all fats and eat more 'whole grains," etc.--you get the picture. So after 15 years of high dose Lipitor, and the false confidence foisted upon him, thinking these pills would prevent further trouble, guess what? He needed a second CABG. Imagine my rage (not at him) as he lay in the post-op unit after the horrific angiogram, knowing I was the one who had to tell him, "guess what?" And his response? "what? but I never missed a day of taking..."
Funny enough, it took me a long time to give up (give up??) my Lipitor dose (apparently a TC reading of 240 was too high for my doctor) and I only gave it up in January when I was diagnosed with occipital neuralgia--a constant, throbbing pain in my head and eye--9 months statin free, I'm finally feeling better. Can I prove the statins caused my affliction? No. But I know from my dad's experience of being on 80--not 60, not 40, not 20, but 80 mgs/day for over 10 years, that these statins are absolutely worthless--and I'm not a scientist, either.
And this is why you're a hero to me.
-Adam
Hey Drew,
Sounds like the 'culprits' are dense LDL, low HDL and low HDL-2b, some RLP and pattern B, characteristic of metabolic syndrome. Niacin only raises blood glucoses in those who still consume excessive dietary carbohydrates, which may only be > 20 grams daily (eg, one bite of a banana or oatbran). Otherwise I NEVER see it go up. Generally I make my patients go as low carb as they can and Paleo (no grains, no legumes, no dairy exc fermented cheeses)
Niacin of course would be beneficial but even more potent for this atherogenic lipoprotein pattern is diet, exercise and correction of any hormone deficiencies (thyroid, vitamin D, etc). Did you have a thyroid panel or vitamin D done?
-G
Adam,
WOW -- Happy Bday to your Dad!!! He's so lucky to have you as a son!
Sorry to hear about the neuralgia and glad to hear it is improved. I work with a Rheumatologist who discontinues ALL statins and other drugs associated with triggering autoimmune diseases (which is nearly ALL drugs). Actually I really had not idea how toxic that statins could be. It does affect the thinking for many people as well (like gluten toxicity) -- changes memory, sharpness, ocd tendencies, mood lability. Cholesterol is very important for myelin sheaths and many other parts of our nervous system and hormone production.
Thanks for you kind words,
G
Thanks Susan.
Dr B.G. Great post! It frustrates me so much that this data is in the published research and my cardiology colleagues are unaware of it. I don't know if they simply do not read anything but abstracts or if they do not read at all. Most of the cardiologists that I know take prophylactic statins (usually samples of brand name potent ones like crestor) and I think it may be making them stupid. I often see them in the physicians lounge eating breakfast cereal with skim milk for lunch looking smug but miserable while I eat real food (anti-inflamatory, low carb,gluten free).
Thank you Dr. Trumbower! Yes, often I feel I live in Seinfield's 'opposite universe'. If the AHA says 8% saturated fat, then I run the other way... 16% or even 24% or 40%! Cut the entire bottom tier of the U.S. Dept of Ag Food pyramid (no grains) and FLIP IT OVER, fats first (40+% of the diet) then veggies and red meat, protein and eggs most days. Three to six! I think all the cardiologists still have positive EBCT scores, at least many of the 'vocal' ones at theheart.org.
Wonder why?? The skim milk and healthy whole grain cereal! (and their prophylactic statin? *haa* that is a good one)
Hi Dr. B G,
Have you met Ron Krauss? He's right around the corner from you. Often these guys give occassional lectures to other professionals. You have to call his secretary and ask. I called Dr. Budhoff's secretary last year and was invited to one of his lectures. I got to talking to him afterward and asked if I could have copies of his various publications. To my surprise he gave me his coauthored 300 page textbook on MBCT's (very interesting).
Anyway, Have you met Ron Krauss? Did you get my email?
Hi Homertobias,
I'd like to me YOU.
*ha* I wish I was at the same Integrative Med conference too. I am impressed by all your posts at other sites we both frequent. Haven't heard yet about Dr. Daphne Miller but I'll search her out soon. I'm going to join a group in Palo Alto with some adjunct faculty who are into all this as well (yeah freaks like us); Dr. Superko's former patient is introducing me. Quite fun! Maybe Miller is already there.
No I've met Dr. Ames but didn't have the foresight to 'set up' at an appt at the same time with Krauss when I was at CHORI. (Ames is like Willett -- not into Taubes). I have a feeling Krauss is different. Right?
You can tell I like Krauss a lot? I emailed his secretary but didn't hear back so haven't pursued further, but I'll try again. Budhoff sounds very cool. Our EBCT owners here in Walnut Creek recently met him.
I'm sorry I didn't get your email. Thank you for your post at Wellsphere. Sorry I have not replied yet --lost my password there.
-G
Just google her. She's got her first book out, "The Jungle Diet" and has a nice practice website.
4 of us stayed in a condo right on the creek, next to the conference hotel. Alot of picture windows of the creek, listen to it at night. 7 AM (groan) Tai Chi, 8 AM -1PM Integrative Medicine Conference (some mediocre, some awesome), 1:30-5:00 hike the Vail Mountains,(georgeous fall colors, lots of quaking aspen), 5:00-7:00 hit the jacuzzi and salt water pool @hotel,(oh my aching calves), 7:00-9:00 Paleo dinner in condo. Complete maid service daily, THEY WASHED THE DISHES DAILY. Can you tell that I am back home now? SIGH.
Vail is not expensive this time of year. List price for a room at Vail Cascade Resort & Spa prior to Labor Day $335 a night. Now $90/night. Condo next door, VRBO, call and bargain.
Homertobias,
OK -- that's why she sounds familiar... the JUNGLE DIET! That's great!!
Aaahhh.... how tempting!! Sorry to hear you are back to reality and no maid-service. I feel our pain.
Let me know your next vacay/retreat!
-G
Hey G,
Just had to let you know that (anecdotally in this case) it looks like you're RIGHT ON about statins preventing a shift from small to large LDL. Here's the story.
You remember awhile back I told you my dad is on simvastatin, but is weaning himself off of it. I've coached him on diet, and he's been eating high-fat/low-carb faithfully for a long time. When he had his heart attack, his calculated LDL was 145 and his HDL was like 31. Trigs were at 150 or so. That was quite awhile back (before TYP or Dr. BG were on my radar ;)), and I wasn't up yet on the NMR, so never had it done back then.
So he's been on a statin all this time (though has been gradually tapering down), and has been doing great on low-carb. 6,000 IU vitamin D per day, 2000 mg niacin, plus a few other supplements including high dose fish oil. You'd think his lipids would be fantastic. So we did an NMR, and here's what we found.
Total Cholesterol: 175
Calculated LDL: 105
Calculated HDL: 59
Triglycerides: 59
Good, right?
And now the NNR:
LDL-P: 1651 (so "real" LDL is 165. Underestimated by 57% per Friedewald)
Small LDL-P: 1568 (so 95% LDL are small)
LDL Particle Size: 19.6 (small, of course)
Large HDL-P: 13.9 (not too bad, as far as it goes)
Large VLDL-P: 0.0
Of course, stupid LabCorp doesn't give any other info about additional HDL subfractions, Lp(a), etc.
Anyway, I thought this was interesting in light of what you've brought out regarding low trigs + statins = sdLDL. Here's my dad, COMPLETELY wheat/grain free, eating a mostly ketogenic diet, next to no fruit, high coconut oil/sat fat for MONTHS -- and still has 95% sdLDL. The only thing I can see that would do this is that dirty statin. Interesting, yes?
Oh, also, he's been supplementing for a few months with 6,000 IU of vitamin D softgels per day (he's about 145 lbs), and his LabCorp result (as of today) was a stinking 32 ng/ml. I told him to bump up his dose to 10,000 IU per day, but wonder if that's even enough. I think his VDRs must be broken or something. lol!
David
David,
Do you think there is a conspiracy? You don't think the statin companies know this?? Krauss has said before that statins NEVER shift to pattern A unless in rare Hypertrig where Tgs >> 400-600. Most MI survivors are like your father, LDL < 100 and Trigs modestly 150-200s and low LOW HDLs.
We have seen this frequently before at TrackYourPlaque prior to conversion to non-statinators. We have a few members that appear to cling-on however. Sadly they invariably report 10-25% persistently increasing EBCT annualized. The sdLDL just hang out at the same level 200-800 nmol/L. No large LDLs to speak of. For those who figure it out, diet fixes in only 4wks. Low low carb Paleo and adding some saturated fats (or a lot). FHC responds excellently.
When I see this, like your father, ALL the LDL particles are small dense. Whatever is left is often Lp(a)! yikes...
No large atheroprotective LDL. Yes Krauss does not feel that lbLDL are associated with risk at ALL, only the sdLDL (I actually edited this post to add but I'll talk again later about that).
For your dad, with all that he is doing with diet and lifestyles and omega-3, all or nearly all of the sdLDL should have shifted out in only 4-6wks. Is thyroid ok?
The Large HDL-P is excellent (statins don't hinder this one until later).
Interesting...
The trigs will improve -- after wt loss and even the ketogenic diets show there is a delay until the Trigs and HDLs really show vast changes. I dunno why for the delay but it makes some sense as metabolism pathways shift too.
Yes -- it appears some 'statin resistance' that Callister, Geiss, Caslake and many other researchers have discovered. Don't worry -- this resolves out in only 4wks if that is the case.
Gallbladder? Perhaps calcified too... Usually digestive enzymes help if the vit D conc does not move in 1-2 mos. He could have started at 10-15 ng/ml which is a common level we are finding.
-G
Good thoughts. Thanks.
I'm guessing that thyroid isn't a huge problem for him, though I could be wrong. He has no problem losing weight, and his TSH is 1.3. I'd prefer that to be a bit lower, and we're upping his iodine dose to see if it helps. Need to get him to take his waking temps to really see what's what.
Here's what's interesting about the vitamin D. When he was originally tested, the cardiologist (Dr. O'Keefe, the famous vitamin D researcher - who should have known better) ordered the test through Quest Diagnostics. The result came back as 41 ng/ml. Dr. Cannell (vitamin d council) recommends dividing any Quest results by 1.3 to get a more accurate result consistent with DiaSorin RIA results. This puts the number at 32 -- exactly what it is now, after months of 6,000 IU per day. So I imagine that Quest waaaaay overestimated the result.
So given his diet, supplements, etc., do you think the sdLDL should have shifted more than it has, even with the statin, or does the statin pretty much explain why it's as bad as it is and make perfect sense of the data?
David,
The HDL doubled with such a wonderful diet, niacin, omega-3 and exercise.
Anything that raises HDL,'should' raise Large Buoyant LDL. That didn't happen -- and that is a side effect of the statin no matter what the dose is when the Trigs are < 180 mg/dl. Sounds like he may have very quickly achieved a low Trig after his event. So the original sdLDL could have been 30-50% higher and yeah -- perhaps the statin lowered it. Now somehow the sdLDL is dialed in and 'stuck'. It seems to me, despite all efforts, drugs, supplements, diet (even low carb) that the dial sometimes stays 'stuck'. I don't know why. CETP drug effects? I kinda suspect.
Until people back off on the statin dose or entirely stop them, it appears to me that the dial maintains the sdLDL population and the failure to produce buoyant LDL. Crestor has a very potent hold on CETP and even causing diabetes; CETP controls insulin. This may be part of its adverse effect profile and keeping a poor inflammatory Pattern B that prevents EBCT regression in those with Trigs < 180 mg/dl. To me that is what the research shows and unfortunately I see several examples of EBCT progression in the statinators of our TYP forum despite all their concentrated efforts, compliance to wt loss/thyroid control/ diet/ exercise and optimism.
Your father has Lp(a) right? Has that improved?
The TSH of 1.3 can be misleading. I totally agree with you -- body temps will correlate better with his thyroid status. Tests for FT3 and FT4 and if you want to get sophisticated the reverse T3 and etc are good too (but I don't know how to interpret yet -- Dr. Trumbower is EXCELLENT *wink*).
I have a friend -- his sdLDL was like your dad's and he has Lp(a). He cut the statin by quite a bit (and every other day) and the sdLDL went to 'none' on the follow up NMR in 4wks.
4 wks!
He had upped the fats (I don't know by how much but apparently enough) and cut out 1-3 servings of carb daily (fruit, barley etc). WOW -- what a difference. 24% sdLDL (triple-digit sdLDL like 170 nmol/L) went to 'none'. His CAC had increased 25% right before this effective intervention; also, he has Lp(a). The thyroid was actually mid-range low -- doc upped the dose of T3 then it overcompensated during the 4wk period (perhaps the saturated fat reduced thyroid requirements? The dose too high?). My friend's Large 'happy' HDL went from 30% to 75% of the total!
You and your dad have done again a STUPENDOUS JOB in a short period in doubling the HDLs!! For regression, esp in the face of Lp(a) like my friend above, Pattern A for the LDL is an absolute MUST and requirement. My friend noticed EBCT progression with only a sdLDL > 150 nmol/L (studies show 300 nmol/L is associated with progression) but he has Lp(a) which accelerates plaque. The large HDL was suboptimal too < 50% which also contributed likely to the progression.
Lp(a) and low HDL2 change everything. Thyroid controls Lp(a)and sdLDL. However, dietary saturated fat controls large HDL2 and Lp(a) AND sdLDL AND increases the mandatory lbLDL for Pattern A.
To me, it's like symphony... Not that hard actually to get harmony and even masterpieces. *haa* Takes a good director to figure out where and how to smooth out discordances. (or to kick out the lame players, eg statins) I think Krauss has figured out how to read the music!
And so have YOU + the optimal solutions!!
-G
Hi David,
Just some thoughts on your dad. Ist low D... Unusual for someone who is not obese. Could there be an absorption problem? As BG says gallbladder? Also celiac panel? I know he is off all wheat but sometimes it takes awhile for the GI tract to recover and start to absorb. Is he on a PPI? The little purple pill wrecks havoc on everything. What brand is the D? A friend's husband is doing D research for the NIH and found great variation in the supposed listed dose. Maybe try bypassing the gut and give him 15+ minutes midday sun to arms and legs daily as well as up his supplements.
The HDL change and the trig change are great. He should be congratulated. No NMR pre MI I take it. Could have been alot worse.
Another thing I sometimes see. Acute illness,surgery, MI's temporarily DECREASE TC and LDLC. There is an increased need for cholesterol to repair cell walls, etc after acute injury. So I was wondering if his first set of labs were just before MI or just after. Makes a difference.
If his doc is wedded to Labcorp,just ask them to run a LP(a). Better still, ask them if NMR lipoprofile will run a lp(a). I have found significant variation in lp(a) levels from labcorp within days of each other and don't know why. Dr BG have you found this?
Wish him well.
Great comments Homertobias!
We've seen variation at TYP but what I really see is that on statins, fibrates, zetia and/or Pletal when the sdLDL is high 50-100%, the Lp(a) particle count [nmol/L] can be high even though the Lp(a) mass appears low < 30 mg/dl.
I suspect the Lp(a) is all small and dense. These individuals will also report EBCT progression > 10% annualized (and of course the LDL is nonexistent like < 60-70 mg/dl). Often probably due to costs, members do not run BOTH a Lp(a) count AND mass at the same time. Ideally both should be if HDLs are low and sdLDL is still high > 10%.
But you are correct, apo(a) has genetic variation and this affects its size (and probably lethality? protection?).
All CKD patients also have higher Lp(a) due to reduced destruction and metabolism at the kidney level -- this promotes along with the mineral disturbances bone buildup in all arteries and organs.
G,
What a fantastic response. You're always so helpful! Thanks.
Yes, my dad definitely has Lp(a). After the MI, it was 225 nmol (O'Keefe was just like, "Doesn't matter. As long as we get your LDL under 70, Lp(a) doesn't hurt you... But take 500 mg of niacin if you want.")
He got on a couple grams of niacin every day, 6+ grams EPA + DHA, low-carb, carnitine, etc., and several months later his Lp(a) was at 192 nmol. Still not very good. Have upped the niacin, but don't know what his Lp(a) is right now (was thinking it would be on the NMR, but LapCorp didn't include it). I'm thinking (again) that the statin might be preventing it from coming down.
We'll definitely be looking closer at the thyroid. My wife and mom are hypothyroid (you'd never know it from looking at them! My wife is incapable of gaining weight), so I'm pretty familiar in a personal way with testing and such.
Another thing my mom told me today (I'm in Texas right now, they're in Missouri, so lots of phone conversations with these new results)is that my dad has been having really bad insomnia lately, and before that, he was waking up every morning at like 4:00 am. So now I'm wondering what's up with that, and am concerned something's getting worse, especially in light of the recent NMR. He had a CABG a few months back (there was some pretty bad scarring from when they put the stents in the first time, causing pretty significant restenosis), so his heart "thumps" a lot when he lies down at night, but it just doesn't seem like it's getting better. THEN AGAIN, he's on lopressor, which can cause insomnia, so maybe that's all there is to it. I'm anxious to get all this figured out and find what works for correcting the sdLDL, Lp(a), etc.
What do you think is the best way cut down on a statin? I've heard of some people shaving a little off their pills every day, while others cut the dose in half every couple weeks. Is there a "right" way to go about it?
(He's a member of TYP, btw, but never gets on there because he's really just not computer savvy at all. Hates computers, and only uses them for writing. I get on there for him and pull articles/discussions for him and my mom to read over and learn from. Even for this limited use, it's well worth the price.)
Again, G, thanks for the discussion.
Homertobias,
Thanks for your thoughts, as well!
We'll definitely be keeping close tabs on the vitamin D situation. He uses Carlson vitamin D softgels, which is a good brand that produces reliable results in others. I have clients that use it with good success, and my mom uses it to maintain at 70-80 ng/ml. I had dad take a 100,000 IU dose today, and then will maintain at 10,000 IU per day starting tomorrow. We'll retest in a month or two to see where things are at. If no significant change, we'll know something else is up.
No, he's not on any PPIs. His digestion works beautifully in every respect, as far as I know. Haha.
He's never had any digestive difficulties with grains, and was actually always really healthy in every way I can think of pre-MI (which is common for Lp(a) types, I suppose). He could have been a "silent" celiac sufferer, I guess, but it's hard to say without the celiac panel, which he's never had. Absorption doesn't seem to be a problem for a lot of other things he takes. This is a thoughtful suggestion, though. Thanks.
No NMR prior to the MI. As I told G, it wasn't really on my radar back then, which is regrettable. The calculated numbers I referred to above (HDL 31, LDL 145, etc.) were post MI. Numbers have steadily dropped from that point with the Friedewald test (except for HDL, which has gone steadily UP).
I need to have him get another Lp(a), but want to keep using the nmol value to stay consistent with what we've done already. Quest does nmol, while LabCorp does mg. Do you know of any direct access labs that use Quest or measure Lp(a) in nmol? I've called around with some of the ones I've used in the past, and they all measure in mg.
The nurse really fought the request for the NMR last time, even ridiculing the suggestion. But the doc eventually conceded.
Thanks again for the thoughts.
David
David,
Carlson's is an excellent brand. I buy their 4,000 IU D gelcaps on iherb at a discount. I subscribe to three rating sites which among other things review supplement quality and it consistantly gets a good mark. CABG's often work well and can give someone "a new lease on life". (Really) Stents often fail. So reassure him. Sleep is so important. You've done a great job for your dad.
My problem with lp(a) at Labcorp.
Same patient, 2 or 3 days apart, lp(a) 44 then 60. So how can anyone tell if a reduction is real or just lab variation? Reproducibility appears to be a problem.
According to the American Heart Association, heart disease is the nation's single leading cause of death for both men and women. At least 58.8 million people in this country suffer from some form of heart disease.
And on the whole, cardiovascular diseases (the combination of heart disease and stroke) kill some 950,000 Americans every year.
Still, there are many misconceptions about heart disease: "The biggest misconception is that heart disease only happens to the elderly," said Elizabeth Schilling, CRNP with the Center for Preventive Cardiology Program at the University of Maryland Medical Center.
In fact, according to the American Heart Association, almost 150,00 Americans killed by cardiovascular disease each year are under the age of 65. And one out of every 20 people below the age of 40 has heart disease.
So, it is now a wise decision to keep a constant monitoring of your health. Why to take a chance if we have the option. I was in the similar misconception that heart disease are far away waiting for me to get aged. But to my surprise, I was found to be having a calcium deposit in my coronary arteries. I need to have my advance diagnostic scans due reassure whether something really deadly is waiting for me. Though it was some dreadful going on in my life, but I never felt any kind of discomfort in Elitehealth.com advanced diagnostic facility. They were having some of the latest diagnostic equipments and non invasive techniques which made me feel safe.
G, very nice post.
Too bad the "cling-ons" at TYP are dominating so many discussions there. I'm really turned off by it.
Acanthusbk,
I appreciate your comment and ALL your support. Yes, I feel similarly and I'm tired... *haaa* Is that evolution??? Where do stubborn-headed buffalo roam? Oh yeahhhh... they don't any longer...
-G
Acanthusbk and G:
C'mon back to the TYP forums. It's been weeks since we've seen you and both your presences are sorely missed. Just ignore the stubborn ones (and if that includes me, so be it).
BTW, many of those hard-headed and stubborn buffalo (actually the term is "bison") now roam mostly in and around Yellowstone...and they're all grass-fed...and quite tasty too, I might add.
=;^0)
Jeg,
Thanks for your kind words. It does mean a lot since to me there are so few that come out.
-G
David,
Your father is doing SO so well! The heart palps are certainly something to think about -- are they new onset? are they related to certain foods: carbs, fats, acidic (tomatoes, citrus)? are they related to medications? Only a trial of changing the timing of medications would be able to yield some meaningful correlations. Certain meds should obviously not be abruptly stopped b/c they can induce withdrawal syndromes (like the beta blocker Metoprolol which are gradually titrated off if necessary).
Statins can be stopped at anytime. I see side effects statin-related probably 25-40% of the time. Some are subtle (like erectile dysfunction, insomnia, memory-loss, depressed mood) and others are more definitive (uni- or bilateral joint ache/pain/soreness, tingling, nerve pain, diarrhea, constipation, etc).
The most common reason for refractory elevated sdLDL (and Lp(a)) is untreated hypothyroidism. I would say actually that ALL (yeah 100% all) subclinical and clinical atherosclerosis is related to hypothryoidism. No one has perfect thyroid and metabolic function at this time (and probably incl me). The oxLDL from our poor, nutrient-depleted, refined diets, environmental exposure (halides) snd goitrogens, over 10-50yrs appears to be related to this pandemic of hypothyroidism.
Ck body temps, consider some adrenal/thyroid support, Armour Thyroid or OTC dessicated porcine thyroid TABLETS, lots of antioxidants (selenium, zinc, C B E A vitamins and TYP stuff). Some reason it appears everyone thyroid insufficient are equally adrenal insufficient.
A friend sent me this fantastic adrenal and thyroid support site:
Body Temp Monitoring/Correction for adrenal/thyroid function
Nutri-Meds thyroid and adrenal support
I know you know this, the full hormone panel assessment is the best -- testosterone, progesterone, preg, DHEA-S, E1 E2 E3, cortisol (2-4x), thyroid, etc.
Granted with that said, even with a hormone disturbance (or multiple), at TYP I see the sdLDL go to zero to 1-2% with diet alone in only 4 wks -- low low or NO carb and upping the sat fats significantly (as you are fully aware I am sure!).
Please let me know the progress with figuring out the source of insomnia or palps. You are right -- beta blockers are associated with insomnia in some folks.
-G
Hey G,
I have not seen you at TYP lately. My reading has been spordiac, and maybe I missed something.
Just wondered how you were doing, and hoping that all is well.
Marilyn
Hi Marilyn,
Thank you so much your kind thoughts! I hope you and your family are doing exceptionally well. I am also very VERY sporadic on the forum as well right now... Feel free as you are aware to continue email.
-G
G,
Another great reply. He's taking metoprolol, but isn't trying to get off of it. I think it's probably good that he's on it for now, since he does have some of the palpitations every now and then. I came back for a visit, and he's doing much better now. No more insomnia, and the palps are less. Seems like it's directly connected to stress, and we've ruled out diet, supplements, etc.
Thyroid. Yep, you were right. Got him to take his morning temps, and they average around 96.5. I took mine as well, and I also come out about the same. A little lower, even. Everybody's got thyroid problems, it seems.
Armour is getting harder to find around here. I've been looking into the OTC desiccated thyroid, and am going to try self-treating myself with it, keeping detailed records of temperature, symptoms, etc. I've seen John Lowe (thyroid guru) talk about a formulation that he thinks works really well. Don't know if you've seen it: http://www.thyroidscience.us/
Here's a good Q&A with Dr. Lowe about OTC thyroid: http://www.drlowe.com/QandA/askdrlowe/desicatd.htm#September 26, 2009
The stuff he recommends is a capsule, however. Do you recommend tablets so the dose can be easily controlled? I don't know which would be better-- the Nutri-Meds or the HSF recommended by Lowe. Looks like the HSF contains more thyroid: http://www.thyroidscience.us/products/hsf/hsf.label.htm
So this is good. We have a doctor locally who is really good with bio-identical hormones, and very open to suggestions. If I suggest to her that my dad would do well on Armour (or something similar), she'd go with it. This gives a new angle to hit this from, which is fantastic. I'm excited to see how this changes things.
He's also upped his coconut oil intake, and puts it in his coffee in the morning.
Anyway, this is good stuff. Thanks again for the great suggestions.
David
Hi David,
Dr. Barnes cautions for thyroid in heart patients who have angina or recently had an event -- since thyroid may 'overstimulate' and make the condition worse. For your father, this may be very important esp in light of the palps that you mention. Barnes advises considering low low doses and instead of titrating every 6-8wks, going even slower every 2-4 months depending on the person and symptoms.
Don't forget to consider for optimum thyroid gland function: Selenium
Zinc
Magnesium (maintain blood upper range of normal 2.2-2.3 mg/dl)
Vitamin E tocotrienol/tocopherols
Vitamin C
Vit ADEK1K2
n-3
B-vits
Vit C
It is so good you are in touch with your body. Actually to hear that your body temps were low. I agree with your assessment -- I guess we are all hypothyroid. I tried for 3-6 mos to sort of chelate out some possible metals and regrow some thyroid gland (*aaahh* if that is possible) and my temps have increased from 96-97s to upper 97s-low 98s (getting my tooth fixed helped the most).
Several of our TYP members use the Nutri-Med site. I don't have experience with the one but I'll look into it. Even with Armour changing their formulation, patients likely can adjust the dose based on symptoms, body temps, mood and heart rates.
Did you find the body temp site helpful? I've read DR. Broda Barnes MD and think his work is wonderful, but unfortunately at the time I'm not sure if he was aware of the concomitantly prevalence of adrenal insufficiency going along with thyroid insufficiency.
Tablets allows for tablet-splitting so the dosages can be adjusted. Right now there is a shortage nationally for the smaller strengths 30 and 60mg of Armour.
Thank you so much for the links on Dr. Lowe -- he seems to be quite knowledgeable!
-G
Interesting that you mention the heavy metals. I personally think this is a MAJOR, HUGE problem with endocrine dysregulation. One of my mentors is actually Dr. Dietrich Klinghardt MD PhD, who is one of the world's foremost heavy metal toxicity experts (a bit of an oddball in some ways, but a definite genius in others) He emphasizes the heavy metal problem in relation to hormone problems, and sees great results with his detox protocols. 5’-deiodinase is basically deactivated by many of the heavy metals (especially mercury), which prevents the conversion of T4 to T3. These metals also bind up the hormone receptors, which is of course a problem. I've actually started carrying some zeolite (ACZ nano- Check it out at resultsrna.com) for my clients to address the problem. There's also Klinghardt's basic protocol with chlorella, etc. I put my mom through it over the last year or so, and she feels SO MUCH better. Still hypothyroid, but it's going easier since the toxicity problem has been getting addressed. Klinghardt's protocol is complicated, though, and the ACZ is way easier for people to do, and seems to have good results in the provocation studies. http://resultsrna.com/research/acz_nano_patient_1.php
Since you mentioned antioxidants, what do you think of vitamin E as far as the balance of alpha and gamma tocopherols? The way I learned it, the alpha tocopherol taken on its own will deplete gamma tocopherol, so they need to be taken together. If this is true, here's a good vitamin E supplement that supplies a good range: http://www.iherb.com/Now-Foods-Gamma-E-Complex-Advanced-120-Softgels/299?at=0
Alright, all for now. Talk to you later.
David
BTW, YES, the site about body temps was really good, and the graphs were helpful for helping to discern the nature of the progress (or lack thereof). The adrenal connection is often missed, and only something I've recently picked up on. Another piece to the puzzle. Very good stuff.
Thank you David for sharing your insights! You must have read my mind!! *haa* I am reading up on a lot of 'detox' regimens and protocols for endocrine disruptions (trying to find and address the 'root causes').
You are way WAY way advanced and ahead of the game! I ck'd out DR.Dietrich Klinghardt MD PhD. Yes -- he seems excellent. I agree, we really live in the a toxic environment (even our mouths which contain so much metal and fillings, water, I have flame retardants ALL OVER our new 3500 sq foot house with wall-to-wall, new sofas, years of drinking chlorinated water which I wouldn't even give my 30 galloon aquarium full of FISH...of course blah blah blah ). You do not want to get me started as I have learned about the environmental dangers, unbeknownst to me and MANY OTHER urban mommies who blithely go thru our days blissfully ignorant. *sigh*
Actually the Now Foods, Tocotrienols & E Complex (has some extra selenium in there which we apparently NEED A LOT OF) came very highly recommended from a friend probably as knowledgeable as you and DR. K on environ health and safety topics.
Here is some great info on the family of vit E's that I found helpful. Yes -- I've read the same that gamma should be taken with alpha -tocopherol. There is some science about separating delta and gamma tocotrienol, but I haven't teased all the info out on that yet (you can catch me up later!)
http://www.drpasswater.com/nutrition_library/tan_2.html
I so appreciate your links and info!
-G
Really enjoy reading your informative blog! I've learned a lot but am also confused. You are a strong proponent of high saturated fat intake but there are a number of places in TYP that talk about the DANGERS of saturated fat. I'm trying to change my diet to very low carb but I don't know what type to fat to increase. Maybe I'm just confused and missing something about the different kinds of fat. I'd appreciate your thoughts about the BEST type of fat to include in my new diet. Is it better to go PUFA or mainly SFA? Or is it a mix?
Thanks - Jay
Hi Jay,
The new TYP Diet Part 3 is actually applicable to ALL TYP members though it says it is primarily for Metabolic syndrome, Lp(a) and diabetes. In reality anyone with subclinical vascular disease has metabolic abnormalities. This diet addresses it.
Fat is 40%.
However, you are right -- the breakdown of the fats is not clear. It is also definitely a recent advancement and not included in the TYP book by Dr. Davis.
I promote 50/50. Omega-3 should a tiny portion 3 to 8 grams daily (that's less than 72 calories so I don't even count it).
PUFA should be as minimal as possible as this oil is toxic and associated with derailing genetic expression of vast organ systems: thyroid, metabolism, insulin, obesity, diabetes, cancer, inflammation, blah blah blah. Max n-6 PUFA 3-4% or preferably less (or one must consume more n-3 PUFA to out-balance and sorta 'neutralize' its toxicity).
I'm sure this is not clarifying anything for you... sorry!
-G
You wrote that hormone contraceptives are bad news? I agree, but I was wondering what you suggest as an alternative?
By the way, I have stumbled upon your blog as of this week. I have agreed with just about everything you have said thus far. It is funny how most people who have gone "paleo" have all reached the same conclusions (probably much to Loren Cordain's dismay): that a very low carb, high saturated fat diet works and feels the best.
Hey Katie,
I am in the SAME BOAT.
The funny is that when men and women are 'Paleo'... they are EXTREMELY FERTILE.
Robb Wolf told us a story at the nutri cert for Crossfit that at one point they were seriously considering having ALL WOMEN sign a waiver acknowledging back up birth control might be necessary combined with Crossit. They had like 11 or 12 women ALL PREGNANT at one time (previously several gave up conceiving). My gym diablocrossfit is BABY MECCA right now *haa* (I better be more careful)
Do you read Mark's Daily Apple? Several readers gave some GREAT advice and pointed to some resources like using beads to count the fertile days, etc.
http://www.marksdailyapple.com/dear-readers-2/
(May 19, 2009 post)
I don't have any answers...
It has been a dilemma for me too :) Seriously, I could probably pop a baby out every 18-36mos...
-G
Katie,
You need to get "Taking Charge of Your Fertility" by Toni Weschler if you're interested in a more natural approach to birth control. This is what my wife and I use, and it's great.
http://www.amazon.com/Taking-Charge-Your-Fertility-Reproductive/dp/0060937645
All the charting, taking temps etc, seems overwhelming, but it really isn't hard at all, and you'll get used to it pretty quickly. Most women love it because it puts them in tune with exactly what's going on with their body at all times.
David
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