Take a walking vacation

If you're planning a vacation, why not consider a walking vacation?

The concept is really taking off. All you need is a pair of comfortable shoes and an interesting locale. More and more services are popping up to help you plan fun and interesting destinations and itineraries. One such catalog can be found at http://walking.about.com/od/tours/a/walkingvacation_3.htm

Lengthier walks may require some advance planning and toting some supplies. Don't forget the water!

From a health viewpoint, a walking vacation sure beats the heck out of a cruise that packs on 12 pounds of extra weight from the 24-hour a day buffet. If you're in the midst of a weight loss effort, several hours of walking through interesting locales and scenery can make it effortless.

There's loads of neat places to visit from a walker's perspective. One interesting website is www.waterfallwalks.com that lists trails that provide spectacular views of waterfalls.

Another variation on this theme is biking vacations. My wife and I are trying to set the time aside for a biking tour of wineries in the French countryside. That's our kind of multi-tasking!

"Expanded indications for implantable defibrillators"

So reads the headline on a magazine I received recently (along with thousands of my colleagues) from a major hospital system.

It goes on to say: "In January 2005, indications for implantable cardioverter-defibrillators (ICDs) were substantially broadened [emphasis ours] to include most patients with a left ventricular ejection fraction (EF) of 35% or less. This change translates into a 2- to 3-fold increase in the number of Medicare beneficiariries eligible for ICDs."

Ka-ching!!! Hear the money piling up in the bank?

The device manufacturers are constantly churning data and lobbying for reimbursement to expand the use of their devices to more and more people. Defibrillators in particularly are generally a $25,000 to $50,000 opportunity for the device manufacturer alone, not counting the costs incurred at the hospital for implantation.

Beware. As reimbursement for stents and other procedures diminishes, expect a sudden "demand" for more and more people to get implantable defibrillators. Better yet, stay away from the whole issue by preventing your heart attack.

Get a heart scan--but then don't delay taking action!

I just came from one of the local hospitals after having performed a heart catheterization on a patient I met earlier this week.

Jack had gotten a heart scan a year ago with a score of 246, placing him in the 76th percentile. The "event" rate with this percentile rank is around 3% per year--not very high but enough to pose risk over a long period.

Jack chose to ignore his score. After all, the pressures of work at the University, maintaining his home and yard, etc. consumed all his energies. He came to my office--now one year after his scan--and told me about the chest pressure he was getting. Initially, his chest pains occurred with extended walking. In the past week, however, Jack was experiencing chest pressure with just walking 30 feet.

This pattern of increasing symptoms is called "accelerated angina", meaning that Jack was rapidly heading towards a heart attack. So I advised a heart catheterization in near future.

Jack's catheterization showed extensive plaque including a 50% blockage in the mainstem artery and 90% in the artery to the front of the heart (left anterior descending artery). Jack is going to have a bypass operation tomorrow.

What if Jack hadn't ignored his heart scan from a year ago? Well, I'd be very confident in saying that he would not be undergoing bypass surgery tomorrow.

The lesson: Don't dilly-dally on taking action to keep your plaque from growing. While it's not an emergency, it can easily become one if you choose to ignore your scan.

Feel that nudge in your back?

You feel that nudge in your back? That's your local hospitals competing for your bypass surgery business.

Just this morning while watching a morning news show, I saw three advertisements for hospital bypass surgery programs. One ad featured a man in his 50s telling his story:"The cardiologist determined immediately that I needed a triple bypass operation. My family and I are very grateful to _____ hospital!"

In what other field is failure celebrated so prominently? When I see these ads, I hear "My doctors failed to provide early detection and then prevent what became a life-threatening condition, even though heart disease is a chronic process that requires decades to develop." What if our man said instead,"I had a heart scan and my score was high. So I was shown why I had so much plaque. They then showed me how to control and even reduce the amount of plaque I had. I'm living safely and symptom-free without need for surgery or procedures."

Of course, the hospital is out $60,000-100,000 for the surgery. How else could they afford ad campaigns costing several million dollars a year? See these advertisements for what they are: Marketing generated by profit-seeking businesses competing for your dollars--lots of them.

Throw away total cholesterol!

Richard's total cholesterol without treatment was 186 mg/dl. "That's great!" his doctor declared, referring to the conventional dictum that total cholesterols less than 200 carry low risk. Several fingersticks in a mall kiosk set up by a local hospital to check total cholesterols confirmed Richard's low number.

But after Richard's unexpected hospitalization and two stents for severe coronary blockages, he demanded better answers.

Tragically, the answer was there all along: Despite a "favorable" total cholesterol, his HDL ("good") cholesterol was a miserable 32 mg (ideal >60 mg).

Total cholesterol is actually the sum total of HDL cholesterol, LDL cholesterol, with a contribution from triglycerides. That's why a low total cholesterol can conceal a low HDL.

This situation is quite common. And low HDL is accompanied by a constellation of other undesirable causes of heart disease, most notably small LDL.

Don't accept total cholesterol as your sole measure of risk. It's nearly worthless. If you live in Bangladesh or a third world country, well perhaps that's the best you can get. But if you live in the U.S. or developed world, it's absurd to rely on total cholesterol.

Smart Start not so smart




Kellogg's has crafted a campaign to support the American Heart Association featuring acress Sela Ward. Her attractive face, familiar to many TV and movie viewers, does add a comforting face to their efforts.

What's in this cereal made by the manufacturers of Pop-Tarts, Cheez-It, Rice Krispies, and Chips Deluxe cookies?

There are, indeed, some healthy ingredients: oat bran, potassium; you can even get a version made with soy protein. But there's sugar listed as the second ingredient. High-fructose corn syrup is also listed prominently. (Remember this issue? High-fructose corn syrup causes overwhelming sugar cravings, causes your triglycerides to skyrocket, and is probably among the principal food ingredients that make you obese.)

Upon detailed questioning of my patients struggling to lose weight, this and products like it are often among the "healthy" foods they've gravitated towards. We spend a great deal of time dissuading them of this idea.

A one-cup serving of Smart Start is low in fat (1 gram) but contains 43 grams of carbohydates, of which there are 14 grams of sugar. There are a meager 3 grams of fiber. To me, this sounds like a cupcake.

The Kellogg's people are exceptionally clever marketers. Partner with the American Heart Association and movie stars? Brilliant!

You should trust food manufacturer advertising about as much as you trust drug manufacturer advertising, which is to say not at all.

Kellogg's sold $10 billion dollars of food products last year. They are the world's leading producer of breakfast cereals. They are a leading producer of convenience foods: cookies, crackers, cereal bars, and frozen waffles under the brands Keebler, Pop-Tarts, Eggo, Cheez-It, Nutri-Grain, Rice Krispies, Famous Amos, and Kashi.

Can they cash in on healthy trends? They'll certainly try.

Does anybody have a normal vitamin D level?

We now routinely check everyone's vitamin D blood level at the start of the program. (The measure to obtain is 25-OH-Vitamin D3. This is not to be confused with 1,25-OH2-vitamin D3, which is a kidney function measure.)

Of the 10 people with levels drawn today, none were even close to normal levels (which we define as 50 ng/ml)--not a single one.

The majority were in the range of severe deficiency (<20 ng/ml). Only two had levels in the 30s. None had higher. (Remember: I'm talking about people in Wisconsin, a terribly sunlight-deprived area much of the year. This might not apply quite as vigorously to Florida residents or others in sun-exposed regions.)

Curiously, I've also seen several people this week who had extraordinary quantities of coronary plaque on their heart scans (scores >1000), all of whom had extremely low vitamin D levels. One of these people had fairly unimpressive lipoproteins, with very minimal abnormalities identified. (This is quite unusual, by the way.) It makes you wonder if a profound deficiency of vitamin D is sufficient to act on its own as an instigator of coronary plaque.

The more we examine the issue of vitamin D deficiency, the more fascinating it gets. I suspect we've just scratched the surface and there's a lot more to learn about this tremendously interesting nutrient. Nonetheless, with what we're seeing in our experience, I'm urging everyone to get a blood vitamin D level.

Don't believe your LDL cholesterol!

Harry's case is typical. For years, his doctor told him his LDL cholesterol of 123 mg was okay. But a heart scan score of 490 (90th percentile at age 52) made him question just where his coronary plaque came from.

Lipoprotein analysis told a very different story: His LDL particle number was 2400 nmol, meaning his trueLDL was more like 240 mg, nearly double the value of LDL obtained through his doctor. Harry had other sources of risk, too, but the LDL particle number was a clear stand-out.

Why does this happen? How can LDL cholesterol be so terribly inaccurate?

LDL cholesterols obtained in virtually all labs are not measured, they're calculated. The calculation was developed in the 1960s by Dr. Friedewald at the National Institutes of Health and therefore goes by his name (the Friedewald calculation). Dr. Friedewald derived this simple calculation to permit doctors across the U.S. to obtain LDL cholesterols, which were technically difficult to measure in those days by using measured HDL, total cholesterol and triglycerides.

Doctors were told that the only time that the Friedewald calculated LDL was inaccurate was when triglycerides exceeded 400 mg. So most family practitioners and internists still believe that calculated LDL's are, for the most part, quite accurate.

Nothing could be further from the truth. When LDL's are actually meaured, you find that LDL is rarely accurate. In fact, in our experience, inaccuracy of 30-50% is the rule, sometimes 100%. The one telltale hint that calculated LDL is wrong is when HDL is <50 mg--that's nearly everybody.

So what's your LDL? You won't really know unless it's measured. Our preferred method is NMR (LipoScience) LDL particle number, probably the most accurate of all. Second best: apoprotein B, direct measured LDL, and non-HDL. (We'll cover this issue much more extensively in an upcoming report on the www.cureality.com website in an extensive Special Report.)

Are you the exception?


I read about 40 heart scans this morning. In the stack was a 41-year old man with a heart scan score of 841.

That's terribly high for anyone, let alone a 41-year old person. He's lucky to find out about this before catastrophe strikes.

People like this worry me. In general, we advise men to consider a heart scan age 40 and older; women 50 and older. If there's anything exceptional about your family history or your own history, then you might notch these numbers down another 5-10 years. For instance, if your Dad had a heart attack at age 43, you might consider a scan at age 35. Or, if you've had diabetes for several years and you're a 42-year old woman, you might think about a scan. (Men tend to develop measurable plaque by heart scans 10 years before women.)

There are no hard and fast rules. It's unusual for a male to have a score >0 before age 40. Likewise, it's very uncommon for a woman to have a score >0 before age 50. But there are occasional exceptions--but they can be very important exceptions.

Our 41-year old man with the score of 841, for instance, probably had a high score since his mid-30s. I've seen several women without any obvious risk factors with scores in the several hundred range in their early 40s.

My rule: When in doubt, opt for safety. Every day, I still read about people in their 30s, 40s, and 50s dying of heart attacks. It shouldn't happen.

When in doubt, get the heart scan. The most you'll lose is the cost of the scan and a modest exposure to radiation. If your score is zero, you know you're safe for the next 5 or more years. But if you have an exceptional score at a young age, take preventive action.

Self-empowerment in health: The new wave in health care

Track Your Plaque is just one facet of the broad and powerful emerging wave of self-empowerment in health.

Hospitals, drug and device manufacturers, and the medical establishment don't like this idea. People managing their own health? That's ridiculous! Dangerous! But mostly unprofitable.

Self-empowerment means having easy access to simple, safe, and inexpensive diagnostic tests like heart scans, carotid scans, bone densitometry (for osteoporosis), cholesterol tests, abdominal ultrasound, even brain scans (e.g., CT or MRI) for people with a family history of brain aneurysm.

Opponents of this idea worry about the "false-positives" that come about with broad testing, i.e, detection of abnormalities that are artifactual. Our experience is that false-positives are only an occasional problem with any test. Instead, we find that most people have many true-positives. In CT heart scanning, for example, we find many unsuspected enlarged aortas (potential future aneurysms), valve disorders, and aortic calcium. These are all important in a preventive program. Unfortunately, your doctor's definition of false-positive often means that no corrective procedure or operation is required.

Other evidence that self-empowerment in health is growing:

--The nutritional supplement movement. What better example of power in managing your own health is there than the fabulous array of nutritional supplements available?

--Medications moving to over-the-counter status. Gradually, more and more medications are trickling into availability for you to obtain without a doctor's prescription.

--What I call "retail imaging", i.e. screening ultrasound, heart scans, full body scans, etc. that are available in most states without a doctor's order.

--The Internet. The rapidity and depth of information available on the Internet today is mind-boggling. It will fuel the self-empowerment movement by providing sophisticated information to the health care consumer previously available only through your physician.

--High-deductible health insurance plans. If health care consumers will bear more and more of the costs of health care, they will seize greater responsibility for early identification and prevention to minimize long-term costs.

There are more. But the movement is powerful and broad--and unstoppable. Let the establishment with vested interests in preserving the status quo fuss and complain, just like horse and buggy manufacturers did in the early 1900's when the autmobile came along.
Mocha Walnut Brownies

Mocha Walnut Brownies

Richer than a cookie, heavier than a muffin, brownies are ordinarily an indulgence that leaves you ashamed of your lack of restraint. Have one . .  . or two or three, and you will surely pack on a pound of belly fat.

But these mocha walnut brownies, as with other recipes I provide, will not pack on the pounds. With no wheat to trigger appetite, nor any readily-digestible carbohydrate to generate blood sugar highs and lows, you can have a nice brownie or two or three and nothing bad happens: You don’t send blood sugar sky-high, don’t trigger formation of small LDL particles and triglycerides, you don’t trigger appetite, you don’t gain a pound of belly fat. You simply have your brownie(s) and enjoy them.

Serve these brownies plain or topped with cream cheese, natural peanut or almond butter, or dipped in coffee.


Ingredients:
8 ounces unsweetened baking chocolate (100% chocolate)
4 tablespoons coconut oil or butter, melted
2 large eggs, separated
½ cup coconut milk (or sour cream)
2 teaspoons vanilla extract
2 cups ground almonds
2 tablespoons coconut flour
1 cup chopped walnuts
¼ cup unsweetened cocoa powder
2 teaspoons instant espresso
Sweetener equivalent to 1 cup sugar or to taste (e.g., liquid stevia, Truvía, erythritol)


Preheat oven to 350º F.

Melt chocolate using double boiler method or in 15-second increments in microwave. Stir in melted coconut oil or butter.

In small bowl, beat egg whites until frothy. Add egg whites, egg yolks, coconut milk, and vanilla extract to chocolate mixture and mix thoroughly by hand.

In separate bowl, combine ground almonds, coconut flour, walnuts, cocoa powder, espresso, and sweetener. Mix thoroughly.

Add dry mix to chocolate mix and mix together thoroughly. If dough is too stiff, add additional coconut milk, one tablespoon at a time.

Place mixture in 9-inch baking pan and bake for 25 -30 minutes or until toothpick withdraws dry.

Comments (11) -

  • Stephanie KL

    1/2/2012 5:54:10 PM |

    Does your pan need greasing prior to adding the batter?

  • Jennifer

    1/2/2012 8:16:40 PM |

    They look great, and I'll bet they are darned tasty, but you are also serving yourself a load of PUFAs with these and then you want to top them with more yet.  One brownie, maybe.  Two or three, no way I'd eat that much PUFA, even if it's coming from nuts and not corn or soy oils.    I don't mean to come across as a twit about this stuff, but if you are a "person in a certain metabolic state", like me,  then you have to really look close at these kinds of things.

  • Might-o'chondri-AL

    1/3/2012 11:45:22 PM |

    For Laura (continuation from previous Dec. 2011 thread "Are you hungry"),
    Assume very  low carb & paleo styled dieters are going with high dietary fat to complement reasonably high protein yet some feel weight loss is not enough. Dietary fat is more than a molecule glob we just act on and has signaling properties for our cells. We synthesize distinct fat molecules inside us from different dietary fats by splitting some apart & elongating into new forms.

    Palmitic acid ( palmitate) is what I suggest as involved in stalled weight loss for low carb & paleo dieters since admonishments to eat more fat don't isolate the types of fatty acids metabolic signal cascades. De-novo lipogenesis from carbs forms palmitic fatty acid but some may benefit from restricting other palmitate sources.  68% of the fat "burned" is usually palmitic acid.

    A mitochondria inside a cell has 2 mitochondrial membranes and to "burn"  most fat (like palmitate) inside that mitochondria  2  molecules are involved. A carnitine based enzyme (carnitine palmitoyl transferase, CPT) can only shunt  fatty acid like palmitate into place for "burning" when there is a free unbound CoA (co-enzyme A) to work with.

    A high fat diet frequently ties up +/- 90% of cellular mitochondrial CoA with fatty acid acyls (as acyl CoA). Coconut oil is only 7-10% palmitic acid and some of the coconut oil's other fatty acids do not need carnitine (CPT) to get into place for "burning" inside a mitochondria. In other words coconut oil fatty acids get "burned" promptly and it doesn't tie up much CoA, which leaves more " free" CoA for other fatty acids to use in order to get into place for "burning". This is part of how coconut oil boosts fatty acid oxidation.

    High protein intake (over time, not as a single meal response) influences the mitochondria;  but let me specify first how it affects skeletal muscle mitochondria. In the inner mitochondrial membrane there is uncoupling protein 3 (UCP3) that is upregulated from a high protein diet. The U.N.'s WHO sets minimum daily protein requirement at 0.85 gr protein/kg. body weight & thus 1.7  - 2.0 gr protein/kg. body weight is a practical description of  high protein  (note: chronic kidney disease and some medical conditions are decidedly not suitable for high protein intake).

    Skeletal muscle UCP3 doesn't work to lower a mitochondria's membrane potential and as such doesn't make that cell use more oxygen. UCP3 causes a type of "uncoupling" whereby it "spills" some protons from the mitochondria's electron transport chain of ATP energy production and results in fatty acid anions (ie: fatty acid hydrolyzed be mitochondria UCP3 splits off a proton). Then that fatty acid anion can fit being shuttled back out from inside that mitochondria to ease the mitochondrial fatty acid burden.

    The effect here, from high protein increasing UCP3 expression, is to "free" up a CoA for each fatty acid shunted out and this then gives that mitochondria more "free" CoA that can then be put to  work with a carnitine enzyme (CPT) to put some of the backed up fatty acid load into position for "burning" to make ATP energy. This is part of how high protein diets increase fatty acid oxidation in skeletal muscle.

    Now, back to palmitate as a dietary fat; consider these food choices where 150 gr. liquid non-fat Kefir = 18 mg. palmitic acid vs 150 gr. liquid regular milk = 1,500 mg & then also compare 150 gr. of cooked garbanzo ( basis of hummus) = 300 mg. palmitic acid vs 150 gr. beef jerky (an example for solid meat protein) = 1,800 mg. palmitic acid. Since when one is trying to lose weight often the desired fat tissue signalling lipo-kines are not doing what normally would .

    Dieters adipose tissue often begin with altered lipo-kine expression and demonstrate multiple gene expression peculiarities that persist even when they have already lost a good bit of weight. Palmitate is implicated, for example, when low circulating adiponectin levels are problematic.

    Aside from the negative effects of the palmitate derivative ceramide (not detailed here) there is the risk that high palmitate interacts with the local inflammatory cells' TLR4 (toll like receptor) engaging NFkB (nuclear factor) causing that cell's enzyme NADPH oxidase to generate excessive reactive oxygen super-oxide molecules. One unknown is whether an individual is vulnerable to any side effect(s) or if  local tissue responds "normally" to elevated levels of palmitate by using the super-oxide spun off as a signaling molecule for a proper metabolic response.

    One concern is that some people with elevated palmitate might get increased endoplasmic reticulum (ER) stress ( ER inside cell is where proteins must fold properly). Doc's readers know we vary in ApoE genetics; and some ApoE isoform % heritage is one reason high palmitate makes them more prone to induced ER stress in certain tissue cells.

    Hunter-gatherer & pastoral people respond to high fat diet with sleekness because high saturated fat over time (not a meal) causes the mitochondrial membrane (paradoxically) to actually become higher in % of polyunsaturated fatty acid (PUFA) content than a low saturated fat intake does. Anyway the result is a more flexible mitochondrial membrane for responding.

    Their proclivity toward high fat fuel "burning" (hunters prefer the fattest parts & herders get lots of milk fat) initially makes that mitochondria put out  lots of super-oxide which becomes a hydroxyl radical that snatches an atom of hydrogen from a PUFA  in that phospho-lipid mitochondrial membrane. Then that metabolite becomes a carbon cored fatty acyl free radical which the cellular oxygen makes into a per-oxyl, which becomes a substrate for spinning off molecules called alkenals (ex: 4-hydroxy-nonenal).

    In the liver (and some tissues) a different type of UCP in the mitochondrial membrane "normally" responds to the alkenal signal  & then UCP 2 "uncouples" to varying degrees of severity so that protons shunting through the electron transport chain (ETC) "spill" protons. In this case the result of upregulating UCP2 in the liver due to a high fat diet is to make the ETC lose efficiency (due to "spill" lessening proton force ) and  that mitochondria must use more oxygen working more to churn out the correct amount of ATP downstream. If one's genetics somehow stymie the increase in UCP2 in any one of the tissue groups with UCP2 function in that inner mitochondrial membrane then high fat intake itself doesn't necessarily trigger this beneficial adaptative response.

    The "normal" side effect from this in the liver cell is reduced mitochondrial  membrane potential from the UCP2, but increased "burning" of fat there; so the hunter (or pastoral) stays sleek because this set up tends to make one lose weight and also keep liver metabolic rate up as they age.  Meanwhile UCP2 alters the dynamic so that less ROS is generated at the mitochondrial staging complex 1; it is a type of self regulatory feedback arrangement where the signal is in reaction to high fat intake. I suspect epigenetic insults to UCP2 may also confound the efforts of some dieters.

    To complete the picture it is relevant  that a high protein diet also upregulates UCP2 acting in key mitochondria; although skeletal muscle UCP2 is not as strongly influenced by high protein diet and it has more response with UCP 3 (skeletal muscle has more of it to begin with) . Our ancestors were feast or famine prone and caloric restriction is another factor which increases both UCP 2 & UCP 3 levels. Thus agriculturists which didn't/don't over consume usually stay slim despite carb based diets & more carb driven de-novo lipo-genesis of palmitate ( with Doc's supplements my labs are good seemingly eating  120+ gr. carbs daily).

    If I were stalling on  low carb/paleo-ish diet I would consider adding in olive oil because the oleic acid counter-acts the action of  palmitate (ex: eat hummus made with olive oil).  Cutting back on palmitate intake conceivably could be off-set by experimenting with more coconut oil (not to be confused with palm oil)  and/or adding in more select nuts/seeds for fat. I would also break ranks with theory and try a protein spell without animal/fowl fat by substituting casein (ex. fat free kefir/yogurt quark) & fish (while keeping up fish oil) & moderate daily portion of hummus to keep protein high (assuming no health contra-indication).

    Excessive (moderation is an individual variable) intake of alpha linolenic acid (ALA) actually decreases the amount of circulating DHA long chain PUFA synthesized and makes less available to incorporate into the cellular membranes. The role of DHA in cell membranes is beneficial for metabolic signaling ; membranes are not just casings of a uniform bagging. So replacing dietary palimitic acid fat with almonds (no ALA, 9% saturated) or sesame tahini (no ALA, 13% saturated), as opposed to loading up on flax (57% ALA, 9% saturated) or walnut (7% ALA, 16% saturated ) or canola (10% ALA, 6% saturated)  for fat may help contribute to other fatty acid signal cascades that might bump one past a weight stall even if already taking maximum fish oil.

  • Dr. William Davis

    1/4/2012 1:40:30 AM |

    Depends on your pan, Stephanie.

    I usually do not and it comes out just fine. If you are uncertain, coconut oil works best.

  • lola

    1/5/2012 4:54:42 AM |

    WOW - I am going to have to read this multiple times to absorb.. ha - but thanks... interesting

  • Ronnie

    1/6/2012 12:31:26 AM |

    I know low carb is the way to go for all genotypes, including Apoe 3/4 people.  But I've read that LOW fat is also necessary to lower heart disease risk for these 3/4's, not moderate fat.  Do you agree?

  • the internet

    1/9/2012 5:01:47 PM |

    ronnie, you cant go low fat and low carb simultaneously

    a diet that was 80% protein would kill you

  • Judd

    1/16/2012 10:34:02 PM |

    Hi,

    Just made these brownies.  Seems like the recipe could use less flour in order for it to be not so firm and dry.  Or increase the amount of coconut milk in the recipe.  I had to use a whole can of coconut milk and some water and regular milk as well to make the consistency to where I could spoon it into a pan.  Tastes and smells great so far...Thx

    Judd
    AZ

  • Judd

    2/9/2012 3:08:24 PM |

    Can''t get these to come out right.  Too dry even with half the amount of flour.  As soon as I add the egg chocolate mixture to the dry, it just all drys up.  Any bakers or ideas out there??

    Thanks, Judd

  • Dr. William Davis

    2/12/2012 2:56:45 PM |

    Try adding more liquid, e.g., sour cream or coconut milk, until you get a moldable dough consistency.

  • Eric C

    2/14/2012 1:58:19 AM |

    Dr. Davis,
    I''d like to add to the PUFA (aka: nuts) restriction argument here. When I initially started low-carb, I ate a lot of nuts. But nuts have a few problems:

    1. Copper
    2. PUFA
    3. Phytosterols

    There are more problems. But increasing copper & PUFA levels in the body causes big problems in the long-term since these two react so readily. After a year or two of eating maybe 50-100g of various nuts per day, my congenital bicuspid aortic valve developed a murmur and mild heart enlargement due to my aortic valve becoming moderately-severely stenosed. The cardiologist I visited thought I would need surgery and/or "wouldn''t make it past 40" without surgery. But I changed my diet. After increasing my grass-fed butter (saturated fat), beef tallow, etc. (low omega-6) fats and restricting PUFA to a bare-minimum (in addition to a few other things, though), the murmur is actually going away. It''s almost gone. I''m only 30, though. I can''t believe it. I was in serious condition just by eating 50-100g of various nuts per day... (odd since most studies show "benefit" on HDL/LDL). But now I''m realizing that despite an improvement in ratio of HDL/LDL, nuts increase lp(a) and oxidized LDL in the long-run like no other.

    PUFA''s are dangerous in excess. I avoid them like the plague now.

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