This is a calculator that finds out the optimal nutrition ratio and amount of food you should eat for your weight loss / maintenance goal. It includes a nifty prognosis chart at the bottom, once you’ve filled out everything.
All of the formulas and calculations are based on the most up to date research I could find. I have discussed most of the calculations at length in the /r/keto forum, where quite some scientific knowledgeable people hang out.
To the best of my knowledge, all the calculations are correct. Keep in mind that the data is based on the average person. Each individual is different, so the results might not be optimal for you.
In short, the only important factor is how many LDL particles (LDL-P) you have. Period. The parameters LDL cholesterol (LDL-C), Triglycerides, particle size matter only because they influence particle count (see below). When you have too many particles, you are at risk. If you do not know your LDL particle count, you simply do not know if you are at risk.
The ideal LDL particle concentration is below 1000 nmol/L. Above 1600 nmol/L means high risk.
That being said, a good predictor for LDL particle is the HDL to Triglycerides ratio. 1 is perfect, below 2 is good, above 3 means significant disease, above 5 means you will explode any moment.
How are LDL Cholesterol, LDL particle size, Triglycerides, and LDL particle count related?
Imagine your bloodstream is a highway. You want to move a given number of passengers (called Cholesterol) from A to B, with as few accidents (crashes into your artery wall that build up plaque) as possible. How can you do this?
When you have only few passengers (low LDL-C), you can get away with using small vehicles (small LDL-particles) to carry them because this will not lead to lots of traffic. When you have lots of passengers to move (high LDL-C) and still use small vehicles, you will need lots of vehicles (high LDL-P) hence get lots of crashes (increased risk of CHD).
When you have few passengers (low LDL-C) but large vehicles that can carry lots of passengers, your highway is empty and you will have hardly any crash. You can also get away with lots of passengers to move (high LDL-C) when your vehicles are big enough that your LDL-P stays reasonable.
Now this is not the whole story. We got other passengers as well (Triglycerides) who want to be moved around as well. These guys take away precious seats that could otherwise be used to carry cholesterol. When you have lots of Triglycerides to carry around you will need a higher number of vehicles to carry the same amount of cholesterol. Again, more vehicles means higher risk, so high Triglycerides drive high LDL-P.
I have been playing around with compression tools for quite a while, and FreeArc is one of the best of the bunch. It has the best compression / runtime ratio of any compression tool I know. Here are two parameter sets I especially like:
uses 4 cores to the max on a 4GB RAM machine, ~10MB per second. Compression ratio is usually above 7z max, while beeing much faster. Decompression is very fast.
A ketogenic diet can help with a lot of neurological problems. It does not work for everything, but it clearly seems to be good for you in the long term.
Epilepsy: KD works very well. That is now no more doubt about that.
Aging: with the KD, rates of degeneration of certain neural structures and functions might be slowed. KD is likely to involve other neuroprotective mechanisms that could ameliorate pathological aging.
Alzheimer: Clinical studies to date have been equivocal but promising. Recent studies have shown a closer linkage of AD to epilepsy. there is growing evidence that the KD may be an effective treatment for AD through a variety of metabolism-induced mechanisms that reduce oxidative stress and neuroinflammation, and enhance bioenergetic profiles – largely through enhanced mitochondrial functioning
Parkinson: a small clinical study demonstrated that 5 of 7 affected patients showed improved scores on a standard PD rating scale. However, a placebo effect cannot be ruled out.
Amyotrophic Lateral Sclerosis: Administration of a KD to mice led to both histological (higher motor neuron counts) and functional improvements. However, the KD did not extend survival time.
Cancer: Theoretically, depriving rapidly dividing, highly metabolic cancer cells of their usual fuel supply, e.g., glucose, could be clinically therapeutic. Animals with experimentally produced brain tumors placed on a KD exhibit markedly decreased tumor growth rates, and these remarkable effects appear to be a consequence of calorie restriction (i.e., reduced blood glucose levels) rather than KD-induced ketosis (i.e., fatty acid oxidation) as the principal mechanism. A pilot trial of the KD in 16 patients with advanced metastatic tumors, six individuals reported improved emotional functioning and less insomnia. It may be that distinct tumor types within different organ systems may respond differently to the KD or other dietary treatments.
Stroke: To date, no clinical trials of the KD have been performed in patients with stroke, but several animal studies of hypoxia-ischemia support the potential beneficial effect of the diet.
Mitochondrial Disorders: KD was both safe and effective in 14 pediatric patients with established mitochondrial defects in complexes I, II, and IV, all of whom had medically intractable epilepsy. However, KD treatment is not recommended in individuals with primary carnitine deficiencies and fatty acid ß-oxidation abnormalities.
Brain Trauma: pre-treatment with a KD significantly reduced cortical contusion volume in an age-related manner that correlated with maturation-dependent differences in cerebral metabolism and ketone utilization. With respect to anti-epileptogenesis following head injury, the data regarding KD effects are mixed.
Depression: In rats, KD led to a beneficial effect similar to that afforded by conventional antidepressants. No clinical studies have been conducted.
Autism: 10 of 18 autistic children demonstrated moderate or significant behavioral improvement (by a blinded rater) after a 6-month trial.
Migraine: in 1928, 9 of 28 patients reported “some improvement,” although the validity of this clinical study is uncertain and some patients admitted poor compliance. laboratory investigations have found that KD treatment resulted in a significant reduction in the velocity of cortical spreading depression (CSD) velocity in immature rats.