Acid in the blood. Does it go with chips?

I thought I would write a bit about blood acidosis and how it effects the way our bodies function.  Whilst doing my research I came across the following article which said it perfectly so I have precede the relevant bits as well as add a few bits in here and there of my own.  I suggest reading the whole article as its remarkably well researched.

The information adapted from British Journal of Nutrition (2009), page 1 of 10 q The Authors 2009 Diet-induced acidosis: is it real and clinically relevant? Joseph Pizzorno1*, Lynda A. Frassetto2 and Joseph Katzinger3

http://images.yoli.com/BritJournalArticle.pdf

Historic overview
The study of acid–base equilibrium and its relationship to the diet and disease has been a subject of considerable speculation for at least several centuries. But, before the 19th century, little was known about the concepts of acids and bases, and no means were available to quantify the acid or alkaline load of foods, or of the pH of physiological processes. Not until the second half of the 19th century did nutritional science began to develop, and the chemical components of food start to be analysed. During the next half century, a number of clinical practitioners outside of academia began to observe health improvements in their patients from consuming unprocessed raw fruits and vegetables, instead of the processed food which were increasingly becoming the standard fare, and developed the concept that life is an equilibrium between acid and base.

What should also be defined, at least broadly, is the net acid load of the diet, the primary topic of the present paper. Diet net acid load can be estimated from measurements of urinary excretion of ammonium, titratable acids and bicarbonate (called net acid excretion; NAE), or can be calculated from dietary constituents (called net endogenous acid production; NEAP). In general, food contributes a net acid or base effect due to the balance between the acid-forming constituents, such as sulfuric acid produced from the catabolism of methionine and cystine in dietary proteins, and the base- forming constituents, for example, bicarbonate, produced from the metabolism of the K salts of organic anions in plant foods.

With an increasing understanding of acid – base chemistry has come recognition of the significant differences between contemporary diets and diets more typical of Homo sapiens ancestors. Although of course we do not know exactly what our hominid ancestors ate, studies in hunter – gatherer tribes suggest a relatively high intake of plant foods compared with modern-day humans(7). In a recent study estimating the net acid load (NEAP) of 159 hypothetical pre-agricultural diets, 87% were found to be base producing, with an estimated mean NEAP of negative 88 mEq/d. In comparison, calculations from the US Third National Health and Nutrition Examination Survey (NHANES III) found the average American diet to be acid producing, with an NEAP of positive 48mEq/d(8). This represents a switch from the net base- producing diet we ate for the majority of our evolutionary history to the net acid-producing diet we have been eating for only several thousand years. Much of the current research highlights this change and the potential long-term physio- logical consequences of a chronic low-grade metabolic acidosis among those eating the typical Western diet, and the effects of reducing or eliminating this diet acid load by altering the diet or giving base supplements.  “So if you eat a typical western diet, even the one recommended by the medical establishment which is high in grain and low in fat, you are setting yourself up for long term chronic disease, due to increased blood acidosis!”

Is acidosis a real physiological phenomenon?
While acute acid loading may only temporarily disrupt acid – base equilibrium, a chronic perturbation occurs when metabolism of the diet repeatedly releases non-carbonic acids into the systemic circulation in amounts that exceed the amount of base released concomitantly (for example, bicarbonate from combustion of organic acid salts of K in vegetable foods)(11). The size of the discrepancy between acid and base production determines the NEAP rate. To maintain equilibrium when there is a net retention of acid (Hþ), at least three compensatory physiological responses are activated: buffering, increased ventilation, and increased renal reabsorption and generation of HCO32 . The major reservoir of base is the skeleton (in the form of alkaline salts of Ca) which provides the buffer needed to maintain blood pH and plasma bicarbonate concentrations. To some degree, skeletal muscle also acts as a buffer(12). Respiratory ventilation increases within minutes if the acidosis is great enough, and the kidneys compensate by increasing HCO32 reabsorption, Hþ secretion, and production of the urinary buffer ammonia, all in response to an acidic load.

In vivo studies have generally supported the in vitro findings that acid-promoting diets are associated with both increased Ca and increased bone matrix protein excretion (used as a marker for estimating bone loss), and that neutralising the acid intake with diet or bicarbonate supplements decreases urine Ca and bone matrix protein excretion. “So if you have a high acid forming diet, you are risking osteoporosis!”

How is acidosis normalised?
The normalisation of a low-grade chronic metabolic acidosis has been accomplished by two methods: change in dietary patterns and alkaline supplementation. Dietary factors that affect net acid production include the quantity and type of protein intake, fruits and vegetables and table salt (sodium chloride). Alkali supplementation is generally in the form of potassium or sodium bicarbonate or citrate. “Citrate is the stuff that is rich in lemons by the way.”

Increased fruit and vegetable consumption, as well as K and Mg alkali intake, is consistently associated with a base- producing diet(47). It has been shown that a vegetarian diet has a considerably lower NEAP than both a high and moderate omnivorous protein intake.

In children, a greater protein intake has been associated with greater bone strength, though this effect is negated if alkalinising nutrients are lacking. It should be noted, however, that clearly bone may be influenced by these minerals in ways unrelated to acid–base chemistry.  “So to make sure your kids have good strong bones, they need quality protein and lots of vegetables”

Finally, increasing sodium chloride intake dose-dependently decreases blood pH and plasma bicarbonate levels(52), independent of the partial pressure of carbon dioxide (PCO2), creatinine clearance and dietary acid load(6). This effect may be due to a decrease in the strong ion difference, as total chloride concentration increases relative to total Na concentration, an effect that may increase Hþ concentration(53). Subjects who are particularly sensitive to salt, generally defined as an increase of 3 to 5 mmHg for a given salt load, have more of a metabolic acidosis than those subjects who are salt resistant(54). So, while everyone’s net acid load would improve by lowering their dietary salt intake, some individuals should benefit more than others from this dietary intervention.  “Interestingly sea salt and Himalayan mountain salt, appear to have the opposite affect. So ditch the table salt and if required replace with sea or Himalayan salt!”

Caution using alkali therapy without careful consideration and expertise in subjects with heart, lung or kidney disease is needed. In congestive heart failure, sodium bicarbonate impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption in these patients, which may lead to transient myocardial ischaemia(57). Additionally there may be several simultaneous processes affecting acid– base status among patients with congestive heart failure(58). Similarly, bicarbonate loading may worsen exercise response in chronic obstructive pulmonary disease patients(59). Finally, subjects with kidney failure may develop elevated blood K levels and potentially fatal cardiac arrhythmias if given K alkali salts, or volume overload and breathing problems if given Na alkali salts.
Is acidosis clinically relevant? “Basically, don’t artificially change things, do it naturally with your diet.”

In an examination of over 1000 women between the ages of 45 and 54 years, a lower dietary intake of acid-producing foods correlated with greater spine and hip bone mineral density, as well as greater forearm bone mass, after adjusting for age, weight, height and menstrual status(60). In the Study of Osteoporotic Fractures Research cohort, over 1000 women aged 65þ years were enrolled in a prospective cohort study. Those with a high dietary ratio of animal to vegetable protein intake (a marker for a greater NEAP) were found to have more rapid femoral neck bone loss and a greater risk of hip fracture than did those with a low ratio(61). “A categoric study that shows if you eat too much protein which is acid forming and too little alkaline forming vegetables you are definitively risking a hip fracture.”

Another prospective, blinded study using potassium citrate in 161 postmenopausal women also demonstrated an increase in bone mass over a 12-month period. The authors concluded that ‘as a proof-of-principle study, it demonstrates that neutralization of diet-induced endogenous acid production increases BMD (bone mineral density), thereby proving the concept that such dietary acid loads are detrimental to bone mass and thus constitute a causative risk factor for bone loss in postmenopausal women with osteopenia’(66).

Another area of interest is the use of alkaline therapy for improving muscle function, exercise capacity and reducing age-related muscle wasting. Acidaemia has been shown to increase muscle degradation in patients on haemodialysis(77). One epidemiological study of 384 healthy men and women aged 65 þ years found a higher intake of foods rich in K (fruits and vegetables) was associated with greater lean muscle mass. The authors speculated that ‘this association is likely to result from the fact that the ingestion of potassium- rich alkaline foods such as fruit and vegetables relieves the mild metabolic acidosis that occurs with the ingestion of a typical American diet’, and suggest that it is plausible that age-related muscle mass decline and sarcopenia may be prevented by the appropriate intake of alkaline K salts(78). “So in theory, this shows that it is never too late to improve you bone density, by changing you diet and improving the intake of your alkaline forming vegetables”

Whether neutralisation of acidosis improves exercise function is unclear, with studies demonstrating both positive and negative results. Short-term intake of sodium bicarbonate helped reduce the exercise-related drop in pH, improved anaerobic performance in a dose-dependent manner(80), improved intermittent sprint performance(81) and was of ergogenic benefit in the performance of short-term, high- intensity work(82). One possible mechanism of action is an increase in plasma pH at rest, providing a delayed onset of intracellular acidification during exercise(83), or by providing additional bicarbonate for an increased buffering capacity, as concluded in a trial involving sodium bicarbonate ingestion by elite swimmers(84). Other studies have not demonstrated any effect of short-term bicarbonate supplementation(85). Longer-term studies on the effects of alkali neutralisation on muscle function and mass are presently underway (LA Frassetto, personal communication).  “So if I’m reading this right, it generally means that a low acid, high alkaline diet will not only lower exercise induced muscle acidosis, ie lactic acid build up, it will also reduce the severity of post exercise delayed onset muscle soreness.  I don’t know about you, but I’m all for that!”

Other
There may also be a connection between insulin resistance and acid–base equilibrium, though this relationship is still speculative. Insulin resistance has been associated with a lower urinary citrate excretion, and hypocitraturic patients show greater insulin resistance than normocitraturic Ca stone-formers(86). Type 2 diabetes mellitus has been shown to increase the risk of uric acid stone formation, because it causes a lower urinary pH due to impaired kidney ammonia- genesis(87). This lower urinary pH cannot be entirely attributed to a greater BMI or acid intake, though both are factors in determining urinary pH(88). Finally, in an evaluation of 148 adults with no kidney stones, participants with the metabolic syndrome had a significantly lower 24 h urine pH than those without, with an incremental reduction in pH associated with the number of metabolic abnormalities present(89,90). “Again, as I read this, it basically means, if you have a high acid forming diet, you are more likely to develop diabetes”.

Also of clinical relevance may be the treatment of pain, although it is less well studied. Local tissue acidosis has been documented in patients with complex regional pain syndrome, and leads to increased pain sensation(91). The mechanism for pain sensation may be mediated by acid- sensing ion channels (ASIC), with an increase in ASIC activity in spinal dorsal horn neurons promoting pain by central sensitisation, a mechanism documented in rats(92). ASIC activity may also be induced by NO(93), and appears to be tightly regulated by pH(94). This is an area that lacks significant clinical research.  “Now for me, this one has massive clinical relevance.  “The majority of my clients are in a chronic pain state and are sadly riddled with arthritis. When I assess their diets, they are predominantly very low in fruit and veg, often none, high in grain and high in poor quality protein.  A few simple changes could, based on the above research help to reduce their pain levels.  Of interest is my clients that have a good healthy diet, rich in vegetables and fruit and lower in grains, invariably, respond faster to care, have far less chronic pain and also have less chronic illness, such as cardio vascular disease, obesity and diabetes!”

So in conclusion, there is a lot of toing and froing regarding what is best research wise, although in general it does tend to suggest an alkaline forming diet is better. However, clinically it’s more concrete.  From both my and my colleagues clinical experience a diet rich in alkaline forming fruit and veg, clean protein and fat and low or absent from grains is far better for you.  It assists in steering clear of chronic disease such as heart disease, obesity and diabetes, to name but a few.  Also if you are training/exercising you can train harder and longer if required and reduce the post exercise aches and pains.  One little addition, bathing in Epsom salts also helps to ease muscle aches due to absorption of alkaline salts through the skin so keep this in mind if you are an arthritis sufferer of just enjoy a good gym session.  So in short…. Pass me a courgette, I’m off to the gym to PR my clean and jerk!

Stuart Lawrence BSc(Hons) MSc(Chiro) DC
Consultant Osteomyologist

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