NU's Quest for Carnivory!

[Wotan]

All I can rpeat is what Nu said. I have mentioned before that every time I give blood I am finished within three or four minutes ... some people take twenty. I take one krill oil capsule per day!

PUFA's are magnificiently destructive - especially when heated. They have been implicated in cancer for at least thirty years. If you think you can avoid them look at every label you see and ask what oil is used in every cafe, restaurant, fish and chip shop and "healthy" snacks in supermarkets. PUFAs - all of them. You see vast cans outside these fast food places, all them marked "vegetable oil, high in polyunsaturates"!!

Who remembers the advert in telly with the know-all little brat lecturing the father about some margerine type stuff (F**** maybe) being good because it had PUFAs etc!

My mum still cooks with them because she read they were good for you. My dad, who had a fry-up most mornings, died of liver cancer.

PUFA's are everywhere!!

Eat lard and be safe!!

[NU_nutrition_TS]

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ok, so in practical terms, for those following a non grain, controlled low or vlow C diet, say <100g/day, large O3 supplementation in addition to one or more daily doses of oily fish is not just unnecessary, but likely harmful in the medium to long term.

What I would say is that overconsumption of PUFAs in general increases the risk of various illnesses.

Overconsumption of O3 (or trying to go in excess of daily O6 consumption) is not going to confer any extra health benefits worth the increased risk of internal bleeding!

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Better to increase sat and mono unsat F consumption and reduce fish oil supplementation ?

Better to make total fat intake 50:40 split between saturated and monounsaturated fats respectively with PUFAs bringing up the rear at around 10% (most of that being your EFAs for the day). In fact most animal fats will have something like this split between the fatty acids!

Reduce fish oil supplementation if you are taking them way in excess of the recommended dose (obviously you have a little leeway but taking 10-20 instead of two a day is extreme)!

If you consume the majority of your fats as saturated (or animal fats) they will help with the optimal absorption and assimilation of the EFAs meaning you get a greater effect from a smaller dose.

[Gareth83]

This is one of the reasons I'm trying to record my omega 3 - omega 6 ratio over a week or so but finding it hard to obtain values for certain foodstuffs.

I'm looking to increase saturated fat in my diet and have been thinking of using beef dripping as a simple way to top it up

[NU_nutrition_TS]

If you use the USDA Nutritional Database (or download the FREE desktop version) they split the fat content of all items into SFA, MUFA and PUFA and list each fatty acid with it's physiological shorthand: 18:2 (n-6) which is the main omega-6 fat Linoleic Acid.

Alpha-Linolenic Acid (ALA), which is the main omega-3 fat, is written thus: 18:3 (n-3).

EPA is 20:5 and DHA is 22:6.

With those you should be able to pinpoint how much of each is in each food listed in the USDA database.

For example:

100g of heavy whipping cream has 37g of total fat.
Of that 23g is saturated, 10.7g is monounsaturated and 1.4g is polyunsaturated. I know it doesn't quite add up, but that is how it is broken down in my version of the USDA Nutritional Database!

Of that 1.4g PUFA

18:2 (Linoleic Acid, n-6) is 0.836g
18:3 (Alpha-Linolenic Acid - ALA, n-3) is 0.538g
EPA (20:5) and DHA (22:6) are both 0g

[NU_nutrition_TS]

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Washboard Abs on a High-Fat Diet, No Ab Workouts and No Cardio?

Ok, not on a totally carnivorous diet...but if you read the blog entry you'll get the gist!

Just found the update to the blog entry I quoted earlier in the thread (see above). For all those who are curious and have asked 'what constitutes a high fat diet & what do the macro splits look like' here is the relevant data from one day's eating by Mark Sisson, pictured in the blog entry linked to in the above quote:






Read the whole blog entry here:
http://www.marksdailyapple.com/fitday-results/

[NU_nutrition_TS]

Fifth week in to a plant-free diet and my stats this morning are as follows:

Body weight: 90.8 KG (-1.5 KG from week one)
Body fat: 12.6% (-2.2%)
Lean mass: 79.4 KG (+0.8 KG)
Fat mass: 11.4 KG (-2.3 KG)
FBP @ RPR: 105/67 @ 54 BPM
FBG: 5.2 mmol/L
Ketones: 4 mmol/L


Although there appears to be a significant reduction in body fat over previous weeks (and even a small addition to lean mass), I am not drawing any permanent conclusions as yet. The difference in the skinfold measurement is only in the order of 1-2 mm and could be an anomaly (though I did take the measurement 3-4 times to be sure!). If the reduction holds true in the coming weeks, then I will consider it a genuine fat loss and not just an anomaly or temporary fluctuation. Overall body weight has changed little and remains relatively stable over a small range, which has been usual for me on a low carb/high fat diet for quite some time!

I definitely think that, after dropping all fruit and veg from my diet, that it is more ketogenic than previously and that I am running on the minimum amount of glucose necessary. Energy remains as high as ever and I can carry on a significant amount of physical work in a post-sleep fasted state for quite an extended period. For instance I will skip breakfast and not eat until late afternoon/early evening (and then feast!). This includes heavy lifting (I dug out turf from my garden to create some borders, took loaded wheelbarrows of the stuff to dump and carried another large bag of gravel home from the garden centre!).

I have stopped recording my food intake on my own spreadsheet but have been trying out a website called the 'Daily Plate', which serves the same function but doesn't need me to be quite so 'involved' in working out the calories and macro amounts, so I am less inclined to tinker with my intakes based on what I see that I am consuming as I go along!

I can also put in my daily intake retrospectively at the end of the day so it is then too late for me to eat any extra to make up macro imbalances.

As an example, here are the total calorie intakes for the last few days of this week: 2293, 3172, 3183, 1073. As you can see it varies quite a bit and the last day quoted I only had around a third of the calories of the highest day's intake. This variance (or intermittency) is natural and based on hunger/satiety rather than mental planning.

As an example of typical macro ratios, on the highest calorie day the macros came out as follows: P=20.38%, C=2.04%, F=77.58%. On the lowest calorie day they were: P=46.87%, C=2.25%, F=50.88%.

[NU_nutrition_TS]

I mentioned previously my experience with migraine and some of the possible factors as to why they originally stopped for several months after beginning the low carb diet and how they gradually came back to be a regular weekend long occurrence. After the last experience (a week/week and a half into the no-plant phase of my diet) I have not experienced any further headaches or migraines. This could be because I switched back to decaffeinated coffee or it could be because I am now on an ultra low carb/ketogenic diet. I came across some evidence for the latter on a web blog belonging to Dr Larry McCleary, author of The Brain Trust Program. Relevant exerpts from an article on his website follow:

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Recent insights provided by research investigating the mechanisms causing migraines are beginning to generate new approaches to an old problem. In addition to producing throbbing (usually unilateral) head pain, a migraine attack is often accompanied by nausea, vomiting, sensitivity to light, tenderness over the scalp, and at times a strange visual disturbance called an aura that precedes the headache by about thirty minutes.

Understanding the cause of migraine headache and aura symptoms has proven to be a daunting task. Since the brain feels no pain, the discomfort that accompanies a migraine is believed to arise from both the blood vessels in the brain and the coatings of the brain, called the meninges. For many years, the so-called vascular theory of migraine directed pharmaceutical approaches. It was believed that aura symptoms were due to constriction of blood vessels in the back part of the brain, which then produced diminished blood flow, reduced oxygen supply, and subsequently generated the characteristic visual symptoms of flashing, shimmering lights that move across the visual field. The subsequent headache component was felt to be related to dilation of meningeal blood vessels with an associated release of inflammatory chemicals over their surface.

More recently, attention has shifted from a vascular theory to a neural theory of migraine causation. What acts as the ultimate trigger is unknown, but it appears to be located in the cerebral cortex - the convoluted surface of the brain. There may even be multiple cortical regions that contribute. It is postulated that some perturbing event in the surface of the brain is the culprit, which is followed shortly thereafter by a depolarization (or firing) of surrounding brain tissue that creates an expanding ripple like the rings on a pond when a stone breaks the surface. This expanding wave of depolarization is referred to as cortical spreading depression (CSD). Some researchers believe this helps explain the migraine aura, especially when CSD develops in the visual cortex.

Evidence from a rare type of headache called familial hemiplegic migraine, because of the development of one-sided weakness concurrent with the headache, has provided insight into possible triggers for the wave of CSD. Genetic mutations that result in malfunction of specific ion channels in nerve cells have been identified in this headache variant. When these ion channels undergo periods of decreased function, sodium, potassium and other ions build up where they don’t belong, making the nerve cells irritable and more likely to fire uncontrollably. Such unregulated depolarization (firing) is energetically expensive and results in accumulation of the excitatory neurotransmitter glutamate. This initiates a metabolic cycle that further stimulates nearby neurons, thus creating increased energy demands. As available cellular energy supplies fall, glutamate continues to increase and the cycle intensifies.

This process is reminiscent of what occurs when seizures are triggered. It just so happens that CSD can be suppressed by the continuous use of a wide array of anti-seizure medications. These drugs are effective not only for migraines with aura, but also for migraines without aura. This suggests the possibility that CSD may or may not cause visual auras (presumably when it doesn’t involve the visual cortex).

A report by a physician whose wife suffered from persistent migraines revealed a serendipitous result. Apparently the woman went on a reduced calorie diet consisting of low-carbohydrate protein shakes to lose weight after two pregnancies. Not only did she lose the desired weight, she also 'lost' her migraine headaches.

The relationship between her physiologically induced ketotic state and migraine cessation is reminiscent of the use of ketogenic diets for epilepsy. If the current evidence identifying cortical instability as the inciting stimulus for CSD holds, both triggers (seizures and migraines) involve foci of irritable cortex and would be expected to respond similarly to therapeutic intervention.

Just as occurs during ketogenic dieting, ketone bodies would be expected to beneficially affect the glutamate/GABA balance of neurotransmitters while simultaneously improving the neuronal energy charge. These would act to diminish neuronal excitability and suppress CSD.

So, just as a ketogenic diet can be successfully used to treat epilepsy, it seems they also may work to prevent migraines. Or, just maybe, migraines as well as epilepsy are a consequence of a high carbohydrate diet?

[martinrogers]

I use a certain well known brand of plastic calipers, sold as being accurate.
These have consistently under measured my BF%, yielding a figure of 6% less that a 12 point BF% measurement taken by an experienced gym instructor using professional calipers and with experience of measuring > 5000 subjects.

I've also been advised by numerous sources that the suprailiac (upper right abdom) does not accurately track BF%, instead a single measurement of the subscapular (back) has been shown to be far more accurate, if you are to rely on a single measurement (?)

I would think that variations in measurments will show fat loss/gain.

[NU_nutrition_TS]

I agree that no method of body fat percentage is guaranteed 100% accurate, not even the gold standard hydrostatic method.

If we are indeed talking about the same brand of BF% calipers then I have taken the suprailiac measurement and used a couple of the Jackson-Pollock (not the US abstract painter!) multiple site methods with the same calipers and got results that match pretty closely (perhaps a difference +/- a few tenths of a percentage point).

However, this is why I have been cautious with this sudden change - my BF% as measured by the single site method has remained constant over many months. I'm not so much interested in the actual measurement (which as you say may or may not be an accurate reflection of my actual body fat percentage) but in the continuing trend up, down or stable over a significant period of time.

For that purpose I think the caliper method is better than any of the electronic gadgetry!

[martinrogers]

For all who use these plastic, their BF% measurement could well be substantially higher than they are being led to believe. In my experience I'd question both the accuracy of the measurement derived from those calipers and the level of correlation with other methods being quoted.

I would place far more reliance on an absolute BF% measurement derived using an experienced trainer, as I described in my previous post. Its expensive, but if you really want to know how much fat you're carrying and whether your diet and exercise regime is benefiting or worsening your situation, a monthly measurement is worth it IMO.