PāNu

Reader Stephen is a young man I have corresponded with a few times on the subject of his diagnosis of FH (heterozygous Familial Hypercholesterolemia) and what he should do about it. His TC runs about 467 mg/dl and his LDL about 333 mg/dl. He has a CAC (calcium score) of 16, which is very high for a 24 year old man. This would be at about the 50^th percentile for a 50 year old male on the SAD.

Stephen has of course given me permission to discuss his case here.

This is his most recent email to me:

Hi Dr. Harris,

It's been awhile since I last emailed you about any recent information regarding my heart scan. I also forgot to thank you for your last response and really appreciate the help you've given me. I recently had more lab work done and I am waiting to hear back for the results, although not much has changed since our last correspondence. However, now that I'm back in Dallas for my summer break I was able to get a proper heart scan at the Cooper Clinic. My CAC score was 16. I attended the Metabolism Society Symposium conference in Seattle a few months back and spoke with Jimmy Moore and a few others about my situation and they recommended I send Dr. Davis an email to get his advice on the matter. I recently heard back from him telling me basically that he strongly believes I go on statins while maintaining my current diet. Jimmy asked me to keep him posted about Dr. Davis' recommendations, so I emailed him, and he is now interested in posting a blog about it and asking others for suggestions since he is strongly against statin use. Anyways, I just wanted to update you, since you mentioned an interest in eventually making a post about this as well. If you're interested in having a look at the scan I can send another copy over to you as well as the results of the NMR profile I drew blood for a few days ago. If not, I completely understand as well, you have a lot on your plate as is. Let me know what you'd prefer and I'll do whatever works best for you. I look forward to hearing back from you. 

Thanks again, 

Stephen U.

By now you already know that I personally would avoid statins under any circumstances as they only work at all on heart attack risk via their effects on inflammation. Taking a sledgehammer to the entire cholesterol machinery has all kinds of negative knock-on effects, including promotion of cancer and interference with muscle and liver function, in addition to the accidental side benefit of reducing inflammation. It’s a crude approach, it has side effects that make all cause mortality over long periods of time likely to be worse, and the only group with any demonstrated benefit is men with established disease. The vast majority of those taking statins have no scientific basis for taking them. The rest, including those who have had an MI already, could likely accomplish far greater improvements in health with non-drug dietary measures like improved glucoregulatory control, and avoidance of the Neolithic agents of disease.

Let me summarize what we know about statins

1)   A few older trials show an all-cause mortality benefit to statins in secondary prevention IN MEN (not women). The relative risk reduction is at most about 30% and the maximum absolute risk reduction is about 1% per year. (This means you still have about 70% of the relative risk of dying you had before the drug. Is it possible dietary changes could decrease your risk more substantially? I think so.) Secondary prevention means you have already had a heart attack or been proven to have coronary artery disease (CAD). If you only have high TC or LDL, this does not include you, and this does not include the majority of those now taking statins.

2)   Other trials, especially more recent ones, are less likely to show a benefit, even in secondary prevention

3)   For primary prevention, there is no demonstrated mortality benefit to taking statins.

4)   When there are decreased deaths from cardiac events in primary prevention, there are more deaths by other causes. You may well be trading your heart attack for cancer. Because of the long lead time for cancer deaths, there are good theoretical reasons to believe that over periods of time - much longer than a few years (the length of the typical drug trial) all cause mortality could easily be higher when taking a statin for primary prevention.

5)   When statins do work, they work by accident via their effects on inflammation. The side effects may be related to the lowering of LDL, but the benefits are not. Trials have failed to show the linear relationship between LDL lowering and cardiac end-points that one would expect if the effect were due to the LDL level.

I do not believe in any of the versions of the lipid hypothesis, ranging from Ancel Keys' original idea that cholesterol or dietary fat clogs the arteries, to the currently fashionable one that “small, dense” LDL particles are like microscopic rodents that are designed to burrow under the intima of your blood vessels and kill you.

Neither cholesterol nor any of the lipoproteins nor LP(a) is a "cause" of CAD (coronary artery disease). There is no evidence that “fixing” these numbers is of benefit other than by accident and there is plenty of evidence that you can kill people by trying to do so. 

HDL, particle numbers, particle sizes, LP(a) are all parameters that are more or less associated with CAD. If they respond positively to changes in diet, then they are just covariant with decreased risk of CAD or MI due to the changes you made in your diet. They are not necessarily, and not usually the direct mediators of the decreased risk.

They may track the positive changes you make in your diet, but they are not causing heart attacks any more than shoe size causes height!

You cannot decrease your stature by amputating your toes. Believing any of the lipid hypotheses or the cholesterol hypothesis is the intellectual equivalent of amputating toes to decrease height because shoe size causes stature. 

Correlation is not causation. Causation can cause a correlation to occur, but proof of correlation is not sufficient to prove causation. None of the lipid hypotheses are biologically plausible, and all have failed to be proven despite decades of research and billions in expenditure. 

Say you observe that the neighborhoods that have the most numbers of police on patrol have more crime. A neighborhood in downtown Milwaukee has more than 8 times the per capita police presence than in Sturgeon Bay 120 miles to the north. The crime rate in downtown Milwaukee is also more than an order of magnitude higher. Say the calculated correlation coefficient is .85 – with 0 being no correlation and 1.0 perfect correlation. Is it reasonable to propose we reduce the number of police in Milwaukee in order to effect a lower crime rate? There is a very high (and statistically significant) correlation, but if we think of mechanisms, and how police presence relates to crime, we would probably think that the police are there in response to the crime and are not likely causing it. We might go a step further and say that it might be dangerous to reduce the number of police, as for all we know the city has put them there for good reason, and the crime differential between our two towns might become even greater without them.

In the same way, although high HDL indeed correlates with lower risk of MI (heart attack or myocardial infarction) and CAD (coronary artery disease), when we understand the biology of HDL production, we might be wary of approaches that attempt to increase HDL as if HDL is the agent protecting your heart. It might well matter how we alter HDL. It might be that HDL is high in response to whatever lowers heart attack risk.

It might be (In fact I think it is) that a diet high in saturated fat protects against atherosclerosis and also affects the numerical value of HDL (most of you know it does because you see it happen to you), such that the association of HDL and lower MI risk is because they are caused by the same thing (diet) instead of because one “causes” the other.   

Consider the particle du jour of LP(a). Measured Lipoprotein (a) has a correlation with MI risk. It’s not really that high as a risk factor (not even remotely close to glycated hemoglobin or calcium score), but there is a positive correlation. In an individual human, Lipoprotein (a) could be high as an adaptive response to having lots of oxidized LDL and thereby may indicate you have an atherogenic diet, like the crime ridden neighborhood that has a substantial police presence. Or you could be just born with high levels of LP (a). In the same way a somewhat paranoid and wealthy community has lots of policemen on patrol even though the crime rate is low, you might have patrol cars of LP (a) cruising around even though you do not have intimal damage occurring.

Sidenote: I admit I have a bias towards this interpretation. My Lp(a) level is 85 yet my CIMT* measurement would be normal for someone 15 years younger and my CAC score is zero. Lp(a) levels can be highly heritable, and longevity and freedom from atherosclerosis runs in my family. As Peter would say, some of us may just be born with more sticking plasters, and some of us make more sticking plasters because we have more damage. It should be noted that the best way to decrease LP (a) is increasing saturated fat intake, but also that although there is positive correlation of LP(a) with disease on a population level, there is not yet a shred of evidence that any intervention to modify your LP(a) level modifies your risk. 

The point is that just by observing more police patrols or more Lp(a), even in the context of a true correlation between crime and police and Lp(a) and MI, you cannot necessarily tell why the police are there or why the Lp(a) is elevated. More importantly, the idea that reducing the number of police will reduce crime or that pharmacologically altering Lp(a) will reduce risk may be not only false, but dangerously false. Some neighborhoods need their police, and some humans may need their Lp(a), just like some humans may have more heart attacks when we “help” them by pharmacologically jacking up their HDL. 

This is in fact precisely the story of torcetrapib. This drug cost Pfizer over 800 million dollars to develop. Torcetrapib is an inhibitor of CETP - cholesterol ester transfer protein. CETP facilitates the transfer of cholesterol from HLD to VLDL or LDL. Now, if you believe version 3.0 of the lipid hypothesis, there are these things called “good” and “bad” cholesterol. This is cardiologist shorthand for lipoprotein-cholesterol complexes that cause or prevent heart disease. HDL is the good one and we want it to be high, so it can hoover up the cholesterol from arterial plaque (a ridiculous idea that as Malcolm Kendrick pointed out defies physical chemistry – Ornish’s “garbage trucks”) and shrink them. LDL is the bad one and we want it to be low, as it is constantly fighting to transport cholesterol to the arterial plaque.

Cardiologists and Pfizer actually believe that LDL is trying to kill you and HDL is trying to save you at the same time. They figured, why not throw our pharmacological weight into the fight? If we inhibit CETP, the level of HDL will rise, and the level of LDL will fall. They actually combined torcetrapib with an extant statin (atorvastatin or Lipitor) to really, really get the LDL down as well as the HDL up.

So how did it work? Well, it worked spectacularly. HDL levels soared and LDL levels went down. I mean, we are talking HDL to LDL ratios that epidemiologists and cardiologists would say should reduce the risk of heart attack to zero. There was a glitch, though. Although the HDL and LDL went exactly the way they wanted, the risk of death in the group that got the torcetrapib was 60% higher. The trial was halted early. 

Sidenote: We could belabor the police metaphor by saying pharmacologic elevation of HDL with torcetrapib was a bit like recruiting Alex’s droogs into the police in “Clockwork Orange”. The crime rate would go up with more police recruited from among those who are themselves criminals. 

So do you think it is plausible that LDL causes heart disease and HDL saves us from it? Or is it more likely that these laboratory numbers are merely epiphenomena to the real primary process?

Is it really plausible that our bodies evolved to simultaneously create two substances that are like some perverse yin and yang, with good HDL trying to save us from the LDL that is furiously trying to clog our arteries with cholesterol?

Or is this all a bunch of biologically implausible nonsense? 

Taking all the evidence in its totality, I’ve see no compelling use for statins for anyone if they have truly optimized their diet, and very little even if they haven’t. The benefits of statins are unrelated to their effects on “cholesterol” or lipoprotein levels, are small and are accidental.

The risk/benefit ratio and effect size of dietary modifications are likely to be superior to any of the current statin drugs.

I do believe there are dietary ways that we can minimize the risk of atherosclerosis and other inflammatory processes, minimize the risk of acute plaque rupture and thrombosis if we do have atherosclerosis, and minimize the risk of a fatal arrhythmia if these upstream steps fail 

I don’t believe once you have taken these steps, that pharmacology targeted to “cholesterol” or lipoproteins has anything to add.

I suggest:

1)   Avoidance of excess PUFA in the diet that leads to oxidized LDL and possible endothelial damage

2)   Avoidance of all the causes of leaky gut that may lead to the suite of inflammatory processes known as the metabolic syndrome – avoid excess PUFA (esp. linoleic acid), wheat, and fructose

3)   Plenty of saturated fat intake

4)   If your glucoregulation is impaired, reduce carbohydrate consumption to whatever is necessary to minimize glycation and endothelial damage. Minimize glycated hemoglobin (Hemoglobin A1c) to the degree possible

5)   Replacement of essential micronutrients that may be deficient on the SAD. Magnesium, sunshine, pastured butter for Vit K2.

Those are my general recommendations for everyone.

So what if you have FH? Are the recommendations different?

More discussion in the next post. 

*CIMT is carotid intima/media thickness - easily measured noninvasively with ultrasound and a more sensitive measure of early atherosclerosis than CAC (calcium score) in men under 40 and women under 50.

OK, now Richard has got me to emerge yet again from my hermitage.

You set out to polish a turd and you find a diamond. What are the chances?

To see what I am talking about you simply must read this

Denise Minger is a blogger and obviously talented freelance writer from Portland Oregon who writes a raw food blog. Like Lierre Keith, she is an ex-vegan.

Having always been on the carnivorous end of the spectrum, when I read Colin Campbell's "China Study" I couldn't really get through it. Sort of like the way Richard Dawkins would have trouble paying attention during a lecture on creationism. The thesis is so stupid and implausible on the face of it, he would not get angry, he would just nod off a lot.

Reading The China Study, which asserts that "animal protein" is deadly and causes cancer and heart disease, I just could not muster that much anger. It seemed so totally implausible and full of non-sequiters that I could not take it seriously, any more than one of those "eggs are deadly, eat whole grains" articles on MSN.

Sidebar:

Quote overheard from the latest jackass on NPR plugging their health book -"...surpisingly, when we looked at increasing egg consumption, it was not linked to diabetes!"

Bonus points if you can guess which university spawned this genius...

I actually entertained the idea of finding a copy of the monograph that has all the data the China Study book is based on, so I could see for myself how Campbell cherry-picked the stuff he based his assertions on. But then, I must have realized once again that time is finite because I did something else instead. Long time readers know I am old enough to have a bias against wasting my time.

Fortunately, in addition to being better looking than me, Ms. Minger is younger and less cynical.

Her bias is in a plant-friendly direction, and she took it as a serious matter to see if the propaganda that vegans wave around ad nauseum in support of plants was actually true. So she set out to polish a turd. She expended enormous effort to pore through the raw data that Colin Campbell allegedly based his book on to see if it was really true. Do read her whole article, but here are the salient points:

1) There is actually more evidence to link plant protein to cancer than animal protein, the exact opposite of what Campbell claims

She writes:

when we actually track down the direct correlation between animal protein and cancer, there is no statistically significant positive trend. None. Looking directly at animal protein intake, we have the following correlations with cancers:

Lymphoma: -18
Penis cancer: -16
Rectal cancer: -12
Bladder cancer: -9
Colorectal cancer: -8
Leukemia: -5
Nasopharyngeal: -4
Cervix cancer: -4
Colon cancer: -3
Liver cancer: -3
Oesophageal cancer: +2
Brain cancer: +5
Breast cancer: +12

But what about plant protein? Since plant protein correlates negatively with plasma cholesterol, does that mean plant protein correlates with lower cancer risk? Let’s take a look at the cancer correlations with “plant protein intake”:

Nasopharyngeal cancer: -40**
Brain cancer: -15
Liver cancer: -14
Penis cancer: -4
Lymphoma: -4
Bladder cancer: -3
Breast cancer: +1
Stomach cancer: +10
Rectal cancer: +12
Cervix cancer: +12
Colon cancer: +13
Leukemia: +15
Oesophageal cancer +18
Colorectal cancer: +19

2) There is no clear evidence for animal protein per se being related to cardiovascular disease

3) The alleged green vegetables benefit is largely confounded by latitude

4) Schistosomiasis confounds the colon cancer data and Hep B confound the liver cancer/cholesterol connection

There are many more and her explication of the data is quite sophisticated. Once again, read the whole thing.

But my favorite part is this:

Perhaps more troubling than the distorted facts in “The China Study” are the details Campbell leaves out.

Why does Campbell indict animal foods in cardiovascular disease (correlation of +1 for animal protein and -11 for fish protein), yet fail to mention that wheat flour has a correlation of +67 with heart attacks and coronary heart disease, and plant protein correlates at +25 with these conditions?

Speaking of wheat, why doesn’t Campbell also note the astronomical correlations wheat flour has with various diseases: +46 with cervix cancer, +54 with hypertensive heart disease, +47 with stroke, +41 with diseases of the blood and blood-forming organs, and the aforementioned +67 with myocardial infarction and coronary heart disease? (None of these correlations appear to be tangled with any risk-heightening variables, either.)

If you didn't spot the diamond, read it again. Can you believe it? Campbell makes a lame case indicting "animal protein" that is easily debunked by examining his own data sources. Simultaneously, he has nothing to say about the strongest food association found in the data.

A positive food association.

Positive meaning that food is linked to much higher rates of disease.

An association between wheat and coronary artery disease of +67! (That's  a 67% increase in relative risk the way I read it)  These numbers are some of the highest in the data set, apparently.

So Ms Minger has approached the ugly task of fact checking that obvious self-aggrandizing fraud Campbell, and with pinched nostrils has found us this nice lovely jewel.

She has perhaps found us more evidence suggesting that one of our three neolithic agents is not good for us.

In epidemiology, these numbers are huge. It is a crime to ignore these numbers on wheat.

Which brings me to my final point, one that Ms Minger did not make.

This is all just epidemiology, and epidemiology is bogus. Now, I don't mean it has absolutely no value. It is good for hypothesis generation. It is almost worthless for finding the truth. It is especially worthless the way it is used by hacks like Campbell who are simply trying to sell people a book that tells them what they want to hear. 

What epidemiology is good for is to use it the way Ms Minger has in her investigation. To say, lets look at these data for associations, and from that generate ideas about what causes what. She seems to have done this in as close to an neutral fashion as is possible

To do as Campbell did, or as almost everyone does when they approach epidemiology, and say, "I suspect animal protein is bad, let's see if I can prove that with epidemiology, is quite simply, epistemologically fraudulent. 

This does not get said often enough or called what it really is.

DATA MINING

If you sift through thousands of variables and look for associations, you will find them. It is in fact a mathematical certainty that some of these associations will be "statistically significant (SS)". It is a further certainty that some of them will be statistically significant soley by accident. Some of your SS will be real, and some will be spurious. You will not always be able to tell which is which!

Let me give two real world examples.

The simple one is taken from what I recall from a medical statistics course ( maybe they don't teach this any more?) If you have a panel of laboratory tests done, say a "Chem 12" and there is a normal distribution of test results ( forget about accuracy, precision and bayes' theorem for now) there will be, say, a 5% probability of one of your labs being outside the normal range. When you do 12 such tests at the same time, the probability is very high that at least one of your labs will be outside the normal range, even if you have nothing at all wrong with you, simply as a function of doing so many tests that are independent. It is kind of like flipping an asymmetrically weighted coin 12 times in a row versus just once.

Second example:

You can check out this book. In the late 90's the Motley Fool website had a whole series of formulaic systems for picking stocks. These systems were all based on logical formulae for evaluating stocks and how they might perform in the future, using earnings growth rates, dividend ratios, etc. These systems could perform amazingly for long periods of time, and sometimes looked foolproof. These systems were arrived at by back-testing. Back testing is simple. You just make up a bunch of stock selecting rules, go back to old stock market data from Value Line, and see how the model would perform from the starting date in the past until now. Then, whichever of the 20 or so models you test performs the best with the lowest volatility, jsut use that one.

What could be simpler?

Actually, what could be stupider?

If you test enough investing models this way, some of them will work very well entirely by accident. There may be some models that may work for real, but you cannot necessarily tell them from the ones that are spurious with statistical techniques.

Sidebar: The "dogs of the dow" model is the best known and turned into a dog itself shortly after being popularized. Sheard's models lasted as long as the tech bubble, and then you would have been wiped out. And of course what good is just beating the broad market when the market has gone less than nowhere in 10 years anyway?

The reason an investing strategy arrived at through back testing is bogus is the same reason epidemiology is bogus. It may be appropriate to backtest for candidate strategies, but you would then need to prove it prospectively over many years, and even then you could not be certain that it was not a fluke about to wipe out your fortune.

Whenever you read papers that talk about linear regressions, think about these back-tested investing strategies. Multivariate linear regression is exactly the same thing. Some of the significant coefficients will be clinically meaningful, and some will be meaningless accidents. The numbers alone will not tell you which is which.

In the same way as these examples, when Colin Campbell sifts through mountains of data looking for SS associations, and then ignores the ones, (like wheat) that don't fit what he is looking for, we should not be surprised when he finds an association that is SS that support his thesis.

The only way to prove convincingly that animal protein is harmful is to do it prospectively in a controlled trial or to make a well reasoned educated guess with laboratory science evolutionary reasoning and common sense. You cannot prove a damned thing with a data-mining exercise alone. 

When will I start blogging again?

Can't say yet.

I'm not dead, lost, or incarcerated. 

I am very sorry if some think it is is "poor form" to stop blogging for a while. Blogging is (so far) a voluntary activity as far as I understand it. I have seen many of my mentors (Peter and Dr. Mike, for example) go dark for a while as they attend to their day jobs. I have several day jobs, so I'll have to do the same from time to time.

If you feel a sense of abandonment you are definitely spending way to much time on the internet!

I own and am responsible for several business ventures, including a multimodality imaging center I read images for and over 12,000 square feet of commercial real estate. I even have some timber. These businesses are simply overwhelming me with work right now and I simply need to do what needs to be done.

Mark Sisson and I have spoken about self-publishing and he has been generous in offering me some advice. So has Dr. Mike. Thanks to both of them.  However, Mark is not "helping me write a book". I wish I were writing a book right now, but I don't even have time to read much.

I am not running a social experiment to test the tolerance of readers or the persistence of blog subscribers. It is however both interesting and gratifying that blog traffic is still healthy and there are now 2200 subscribers vs 2000 3 months ago. Visits are still at 170,000 a month. This might relate more to the writing than its frequency or volume, I would reckon. I'll continue to write when inspired and not when I have nothing to say.

Substantive posts will definitely return some time. 

In the meantime, there will be no fluff. I don't do fluff.

You may continue to use the forum bandwidth on my dime, but I may only occasionally check in to see any complaints.

Thanks to you all for your patience and concern.

I'll definitely return but can't yet say when.

 Meleagris Gallopavo Silvestris is an animal well known as a food source exploited by native americans. The weak and flightless albino CAFO animals we Americans eat by the millions on Thanksgiving day are a mutant version of this magnificent wild bird.

As a game species, the wild turkey is big enough to be exciting and offers enough meat to be worth the effort to hunt. But you don’t need a truck to bring it home (like whitetail deer) or a helicopter to retrieve it from a swamp (like a moose in Maine, for instance)

You can look at the map and see that the eastern turkey –silvestris - is available to hunt for most of you that live east of the Missisippi river. The other varieties are found in the western states and Mexico, but silvestris has been transplanted in the west as well, including to California. Wild turkey populations are booming all over, with such robust populations that you can get several tags (and thus kill more than one bird per season) in many states.

Blue silvestris   - Eastern Turkey

Orange Osceola      - Florida Turkey     

Green Intermedia  - also known as Rio Grande

Red Merriami      - Merriam’s

Tan Mexicana     -  also known as Gould’s

As a youngster, I went hunting a few times with my father for phasianus colchicus (see photo below), but not often enough to be successful at it. I can’t really say what kept the flame lit, but I still nurtured a desire to hunt as an adult. In my early 30’s I started in with a variety of shotgun sports, including, trap, skeet, and sporting clays. I had a brother-in-law that came back to Iowa to hunt every fall, and with his inspiration (thanks, Doug) soon I was hunting pheasants every chance I could on local farms in the Iowa City area. My most successful season I managed to bag 27 birds with no dog to point or retrieve. The secret to preparing pheasant is to gut the birds and age them in feathers at refrigerator temperature (35-45 degrees F) for 4 to 5 days. That is why you see the birds hanging in the three-season porch.

The ringnecked pheasant is an asian import that has thrived in the upper Midwest of the US since being introduced in the late 19^th century as a gamebird. As writer Datus Proper has said, pheasants are wild birds that thrive in the interstices of agricultural civilization. They live in the weeds that grow between plots of the farmer’s corn that they eat. Shooting pheasants is wingshooting, where you use a shotgun to kill birds as they fly. With big rooster pheasants weighing up to 3 pounds, they are tough birds to kill. An ounce and quarter of hardened shot from a 12-bore shotgun is advisable.

The wild turkey is a bird that is related to gallinaceous birds like pheasants and chickens, but its size and the hunting techniques used really put it in the category of big game. Although wild turkeys can fly quite competently (I’ve seen them fly well over a quarter mile at a time) turkey hunting is not wing shooting. Male turkeys, called Toms or Gobblers, can weigh 25 lbs or more, which is ten times the mass of a pheasant. In order to kill them reliably with a shotgun, you must get a head or upper spinal cord shot. You need a dense pattern of shot centered on the head and neck. You need them to be standing still or walking slowly when you shoot.

There are a variety of strategies that are used. The main hunting season is in the spring, and as with ring necked pheasants, only males are legal game.

Sidebar: Bird polygamy means populations can be maintained with only a fraction of the males surviving to breed the off-limits hens. In the case of pheasants, you can kill up to 90% of the roosters each season and the hens will still all be bred and the population maintained.

Therefore, spring strategies center on exploiting the capability and desire of the Tom to mate with any and all available females.

Turkeys roost upright and sleep in trees at night (try that yourself some time without falling) If you have a place you can hunt where the turkeys fly down from their roosts at a known time every daybreak, and perhaps travel to a typical location to feed, you can set up a blind to hide from them and wait for them to come to you. When they are in calling range, you can use one of a variety of calls that mimic the sound of a hen. Many use plastic turkey decoys to add to the realism and help attract the Toms. If you sound even reasonably like a turkey, and the Tom can hear you, and he is not too “henned up” (has too many females he is already tending to abandon them to go after your ersatz auditory hen), and the Tom gets within 40 yards of your location and holds still enough for a shot without seeing or hearing you, you can shoot him.

Here is the call I use.

It’s a box call, operated by sliding the slightly sprung top against the edge of the box. I can’t say it works any better in general than a slate call, which is a disc and stick you stroke against it, or a diaphragm call, which takes some skill but has the advantage that both hands are free to shoot while you call. I use it because I killed my first turkey with it last season, and I killed another with it last week, so I suppose we can call it a rational superstition that this is my preferred call.

The shotgun I used this year is a Benelli M2 in 12-bore (pictured in the first photo). The black synthetic stock is impervious to rain and dirt and the parkerized finish on the barrel and receiver is flat. The lack of bright metal and reflective surfaces makes it easier to move the gun without alerting the birds keen eyesight. They make guns covered in camouflage print. You pay extra for such guns. In my opinion, they look ridiculous and probably add to your hunt effectiveness as much as camouflaged pickup trucks or bedspreads.

The load I use is a 3 inch shell with 1 3/4 oz of a tungsten/steel alloy called hevishot in size #6. It is actually denser than lead, which means for a given pellet size it retains more downrange energy. My test patterns give me confidence to shoot with this round out to 40-45 yards. The shot hardness also gives tighter patterns, which is also very helpful in this game. These hevishot shells ( the tan one on the left) cost about $3 US per round. This is not wingshooting, so the expense is meaningless once you have used $15-30 of them to test-pattern your shotgun at different ranges. I have never killed a bird outside 25 yards, though, so a more standard load of 1 1/4 or 1 1/2 oz of lead might have done fine.

I have hunted turkeys now a total of 4 spring seasons. The first season was in 2000, and I was busy so only hunted on one day I had available. I was on a friend’s land and I did not have the advantage of any knowledge or experience with turkeys at the time. I had read a few books (listed at the end of the article) I set up a pop-up blind in what I thought might be a likely spot, and within 15 minutes a hen walked 5 yards in front of the blind. When she was gone, I started calling with a slate call. I thought I sounded like a turkey, and sure enough, I heard a loud gobble from the woods to the north. I would cutt ( a short sound repeated 2 or 3 times) and the Tom would gobble loudly. It seemed like he was only maybe 50 yards away, but now I realize he was more like 125 yards. Gobblers are loud! We went back and forth like that about 20 twenty minutes or so, and he would no move any closer. Sometimes if a Tom hears a hen, he will strut (the sexual display to attract the female) and gobble, and expect the hen to come in to him. I had read as much in my books, so I crawled out of the blind and carefully crept into the woods. I feared I would be seen (thinking he was closer than he was) and only went in about 30 yards or so. I sat with my back to a tree and called a few times. Not hearing any more gobbles in response, I waited about 5 minutes more. Figuring I had been made, I left the woods.

My next hunt was in the spring of 2008. I now had new land to hunt on, and made the classic mistake of looking for my keys where the light was best. I set up a blind in a likely-looking spot, and over several hunts called in vain with no replies heard. The only turkeys I saw were driving to and from hunting.

For Spring 2009 I took my 2008 experience and actually learned from it. I noted before the season where turkeys roosted, and where I saw them when I was out driving, and I made the effort to get permission to hunt on several more properties where I had seen birds. I resolved to use a run-and gun technique, where you attempt to locate turkeys on the fly and if you get no response to calling, you move on to a different area. This is done with no blind and (at least by me) with no decoys. I looked like this:

Camouflage jacket, Filson shelter cloth hat, $5 face net from cabelas and “mechanix” automotive gloves. The gloves and face net are the critical parts. White skin is like a beacon to a turkey’s eyes. (They see color, by the way, so stick with greens and browns)

On opening day, I started by making the rounds of my several properties at about 10 am. The first place I saw birds was along a fence line at the local rod-and-gun club.  I approached the birds from the woods south of the fence line, but was too aggressive and bumped into a jake before I could set up. He startled the other birds and they all flew off, so I packed off to check my next spot, #2. On the road leading up to property #2 was a Tom standing in full strut in the middle of the road. This road happened to border property 3 on the north, so I kept driving at a slow pace towards the bird. When I got about 200 yards away he left the road and entered the woods to the south of this east/west road. I carefully marked his entry point and continued on another quarter mile or so down the road. I parked my wagon and quickly got out my shotgun and trotted back in the direction of the Tom. When I was only 100 yards from where he entered the woods, I cut into the woods about 15 yards perpendicular to the road. I sat with my back to a large cedar in a position like this, with my shotgun on my lap and my call in position:

 I called with two cutts and immediately got a loud gobble from his direction. After a minute, I called again and he responded. Two more times at 30 to 45 sec intervals, and each time he sounded closer. Suddenly I could see him through the trees. He had come out to use the road to get to his “hen” faster. Now that I could see him I stopped calling and just watched, with my gun at the ready like this:

He picked his way towards me in an irregular pattern, stopping to strut in an opening when he was 23 yards away. I fired once and he went down. From seeing him on the road to shooting him was about 10 minutes.

Now, turkeys have spurs (on their turkey “heels”) than can send you to the ER for sutures if you are not careful. Don’t grab him just yet. It’s best to keep a round chambered and stand by. Of course, if he gets up or starts flying, you will have to shoot him center-of-mass. In a few minutes, though a properly head-shot bird will stretch his wings in an agonal spasm and then lie still even if you poke him with the gun barrel. At this point, it is safe to pick him up by the legs and carry him out.

Here is my 2009 bird, weighing in at 21 ½ lbs:

My 2010 hunt was just over a week ago. So I guess that makes this yet another “excuse post”. If your once-yearly 5-day turkey season prevents blogging and makes you lose readers, well.. it is what it is.

Anyway, opening day 2010 I made the rounds at three of my spots using my run-and-gun approach. My third spot revealed two Toms and several hens and jakes in the center of an 80-acre field. Now, anyone who has hunted whitetail deer knows that this is a sucker’s bet. The more visible the prey to the predator, the more visible the predator to the prey. I tried to put the sneak on these birds by crawling on the far side of a tree line bordering the field but the whole flock spooked at my movement when I was still about 100 yards away. The birds were upwind, which is to say, I would have to be close on this very windy day for them to hear my box call. I felt I had to get close as I got no response from the Toms when calling from 150 yards.

The second day, I was actually busy with some other business-related task that escapes me now, so I did not get out until  about 3:00 pm. This time, I made the rounds and saw no birds at any of my spots. So I just set up in a wooded area about 200 yards south of where I always see turkeys roosted in the trees. I sat with my back to a large tree and started a calling sequence – just 2 or 3 cutts every minute or so. After maybe 3 minutes, I got a gobble that sounded maybe 100-150 yards off. We played call-and-response for a good 20 minutes like this, and I could sense a lateral change in direction, but he would not come closer. This was tough. This section of the woods was northern hardwood, with nice, crisp, noisy aspen and ash leaves carpeting the ground. It was very loud to take even a step, but I had no choice. So I advanced slowly toward the gobble by attempting to step on tufts of grass, soggy rotten logs, moss, etc. I took about 10 minutes to move 50 yards. Once I had done so, I carefully repositioned as in the picture above (shotgun on lap with call) and started a few gentle calls.

Nothing.

I waited about 2 minutes and called again.

Nothing.

I waited 5 minutes and called again.

Still nothing.

After 10 minutes of this, I heard nothing. I knew he could be moving without calling back, so I waited 5 more minutes. If he were coming, it seemed he could have easily closed the distance in just a few minutes.

I got up to leave, thinking I had probably scared him off with the ridiculously loud crunching leaves left over from November, and that I had tried to get to close. I stood, slowly and started backing out of my spot, because, well, you never know..

Just as soon as I was fully standing, I head one of those “no doubt about” sounds you hear when hunting. There is absolutely no doubt something is coming, but you have no idea if it is a man, a deer, a turkey, a black bear or the neighbor’s dog.

Swoosh, swoosh..

So I waited. And as I waited, I slowly crouched down into a kneeling shooting position. My visibility was terrible now with leaves literally sticking in my face, but I didn’t dare move again in case it was the Tom.

Swoosh, swoosh..

Suddenly I saw his blue and red head at about 40 yards, off to my far right at a 30 angle from where I could comfortably shoot. The swooshing noise was him dragging his tail feathers over the crunchy leaves. His head disappeared, but now I could hear him moving from my right towards my left. He was zig-zagging looking for the hen he had heard. The next time I saw him his head popped up, facing perpendicular to me at no more than 18 yards, as I paced it off later.

Here he is again, and that's him in the lead photo up above:

Last year, I boiled water and scalded the bird. My wife and I plucked all the feathers and we smoked it in our electric smoker at 225 F for about 6 hours. The bird was a little dry that way, even with the skin on. This year, I gutted and skinned the bird as I would have done a pheasant. I used a hand axe just like in the cartoons to expediently remove the head, feet and wings. Crude but effective. I washed the bird and then put it in the regrigerator in a plastic bag to let is age. A few days later, I rubbed some spices (a variety of peppers and salt mostly) on the carcass, and smoked it for 4 hours at 225 F. Despite having no skin on it, it came out moist, tender and delicious, with the reduced smoking time. I can't claim this method of preparation is the best for fat intake. but I don't view birds as much of a fat source. A turkey could be optimized to get all the fat by saving all the storage fat in the lower neck area and by boiling it and drinking all the stock if you were so inclined. I might try that next year. But this year, the bird came out looking like this. Not the biopsy slice where I cut into the breast to make sure it was fully cooked.

Here is the smoker I use. It a cookshack with a simple  thermostat and an electric heating element. You load a small chunk, say 3 x3 cm, of aromatic hardwood of your choice (maple, cherry, etc.) into the bottom of the unit. At 225, it smokes slowly and flavors the meat, turning into a chunk of porous charcoal in the process. No water, no propane or charcoal and no supervision required.

Using an hours-per-pound-of-meat metric, hunting the North American wild turkey may be more efficient than bowhunting for that other big-game animal, the whitetail deer.

Once you have some idea of what you are doing, anyway.

Other than for exotic table fare, why hunt?

Well, it’s a lot of fun, for one thing. I certainly hunted before I was ever “paleo” and most of the hunters I know in Wisconsin would not dream of venison or turkey without the accompaniment of bread, beer, soda pop and sugary sauces.

I can’t pretend that wingshooting for pheasants or grouse is Paleolithic behavior, as it dates from invention of appropriate arms in the late 17^th century. Shooting a wild turkey in the head with 1 ½ oz of hardened refined lead shot propelled by modern smokeless propellant from a factory made shotgun with a petroleum-derived synthetic stock is not Paleolithic in terms of the technology used.

If you kill a whitetail deer or turkey with a stickbow and string, that is emulating late Paleolithic or early Neolithic activity.

So where is the evolutionary or ancestral or paleolithic part of hunting with relatively modern technology?

Well, first I would say that we should avoid the “man as cancer on the planet” fallacy and the assumption that technology and nature, including human nature, are somehow separate. Tools made by the tool-using animal to accomplish tasks like hunting for food are as natural as any other phenomenon that is real.

Using tools is what makes us human. Maybe this is just what I tell myself because I find the art in weapons like fine shotguns and rifles and bows and knives deeply compelling. The beauty in tools (cars, firearms, hi-fi systems, mechanical wristwatches, computers) is appreciated by many, but tools that can feed you seem to me to be profoundly beautiful in a way that some other artful tools are not.

So I think that using modern versions of hunting tools is perfectly natural and it is still hunting as long as there is enough effort and uncertainty and intimacy in the endeavor.

How do you know if you are using too much tool?  If you hunt, you will know. When you feel no fear or excitement doing it, you are probably not hunting any more.

But I don’t think the technology used is the crux of what we get from hunting. After all, you can roam the woods with an osage selfbow and flint tipped arrows made from phragmites reeds and if you don’t intend to kill anything, you are definitely not a hunter.

The value of hunting is primarily in being honest about where food comes from, and about how we got where we are, while enhancing both the quality of our diets and the quality of our being in the world.

The parts that brings you back to your predator heritage are not dependent on the tool you used to kill the animal at all. That matters to the “sport” or, a misnomer in my view – the “ethical” part of hunting - the part that asks: how challenging was it?

The parts that connect you with the rest of the universe are when the animal dies so that you can live. When you gut it, skin or pluck it, and finally when you eat it

Further reading:

Pheasants of the Mind by Datus Proper (This is the best book on pheasant hunting and one of the best books on hunting period)

Pheasant Hunter's Harvest by Steve Grooms

Turkey Season - Outdoor Life  (This is the best turkey book)

Innovative Turkey Hunting by Jim Casada

The Wild Turkey - Biology and Management  by James Dickson  This is a good scholarly book on turkey biology.

A final caveat. I have an intelligent readership. Many intelligent people under-emphasize experiential learning in favor of book knowledge. You will learn far more about hunting (and about yourself) from getting out there and doing it than you will from any book.

Not abducted by aliens. No anal probes, etc.

Worse.

This is the first tax season I've been through while trying to maintain a blog. With two corporations, two LLCs and a complete set of personal tax returns to organize and file, it is simply not possible to blog during tax season. This is not just a function of time, but of the way the Leviathan state and it's rules and regulations, byzantine, and arbitrary engendered to sow fear and confusion, simply command your attention to the exclusion of all else. Add in computer failures and networking tasks at two businesses, and you end up not blogging for weeks.

In the meantime, one of my first readers, Dr. Jeff Klugman, ran into Gary Taubes at the recent Metabolism Society meeting on the east coast. Jeff had a copy of GCBC autographed by Gary and surprised me with it in the mail.

Thanks Jeff and Gary, you conspired to make my day!

I'll start getting to membership requests and real blog posts again very shortly.