Diamox is a drug that is directly enhancing your performance at altitude = cheating.

Diamox doesn't enhance performance at altitude, it just speeds aclimatization.

Same difference!
The fact is that people take such drugs to compensate for lack of confidence in themselves.
It is unethical and it should be totally unacceptable in the alpine climbing community, period!

The fact is that people take such drugs to compensate for lack of confidence in themselves.

So you know nothing about the subject, you know nothing about high altitude, and you know nothing about mountaineering history. Damn, that's a pretty impressive lack of knowledge.

Diamox is a drug that is directly enhancing your performance at altitude = cheating.

Dex (Dexamethasone) on the over hand is a drug that you can take in an emergency against HACE.

That's a BIG difference.

But hell, if you feel a need to use Diamox you are probably too weak-minded to do any serious climbing anyway, so who cares.

I was recently made aware of the fact that a number of biochemical studies show that Caffeine has effects on the Calcium channel of our cells, and if I remember rightly, the misfunctioning of the calcium channel is one of the primary culprits in the creation of Altitude related illnesses.

No, no, no....the caffeine (or other Calcium channel blocker) HELPS AVOID HAPE/HACE.

Localized alveolar hypoxia causes constriction of the small resistance pulmonary arteries, thus diverting the desaturated, mixed-venous blood to better ventilated areas of the lung. Although modulated by endothelial vasoactive substances, the constrictor response to hypoxia is intrinsic to the smooth muscle cell. Ion channels are important elements in two of the three components of the response. Hypoxia inhibits several potassium channels (voltage-gated and TASK), leading to membrane depolarization and calcium entry through L-type channels. It also causes release of calcium from the sarcoplasmic reticulum, with consequent repletion through store-operated calcium channels. Finally, the effect of the rise in cytosolic calcium is amplified by enhanced calcium sensitivity of the actin/myosin interaction, achieved by the hypoxia-induced increase in Rho-kinase activity. The change in oxygen tension that stimulates these three "executive" components is signaled by a change in the redox status of the smooth muscle cell and probably by downstream changes in G-proteins. Ion channels also play a critical role in the vascular remodeling that results in chronic hypoxic pulmonary hypertension, seen when all the pulmonary vascular bed is hypoxic, at high altitude and in patients with chronic lung diseases. The same inhibition of potassium channels and influx of calcium results in high cytosolic levels of potassium and calcium. These, respectively, lead to inhibition of apoptosis and an increase in cellular proliferation. A better understanding of the pathophysiology of hypoxic pulmonary vasoconstriction and vascular remodeling will enable the design of better treatments for hypoxic and other forms of pulmonary hypertension.

High altitude pulmonary edema (HAPE) is a potentially fatal complication in response to exposure to low O(2) at high altitudes. Hypoxia, by causing pulmonary vasoconstriction, increases pulmonary vascular resistance and pulmonary arterial pressure, both of which are features in the pathogenesis of HAPE. Uneven hypoxic pulmonary vasoconstriction is thought to be responsible for increased capillary pressure and leakage, resulting in edema. O(2)-sensitive ion channels are known to play pivotal roles in determining vascular tone in response to hypoxia. K(+), Ca(2+) and Na(+) channels are ubiquitously expressed in both endothelial and smooth muscle cells of the pulmonary microvasculature, subfamilies of which are regulated by local changes in P(O(2)). Hypoxia reduces activity of voltage-gated K(+) channels and down-regulates their expression leading to membrane depolarization, Ca(2+) influx in pulmonary artery smooth muscle cells (by activating voltage-dependent Ca(2+) channels) and vasoconstriction. Hypoxia up-regulates transient receptor potential channels (TRPC) leading to enhanced Ca(2+) entry through receptor- and store-operated Ca(2+) channels. Altered enrichment of ion channels in membrane microdomains, in particular in caveolae, may play a role in excitation-contraction coupling and perhaps in O(2)-sensing in the pulmonary circulation and thereby may contribute to the development of HAPE. We review the role of ion channels, in particular those outlined above, in response to low O(2) on vascular tone and pulmonary edema. Advances in the understanding of ion channels involved in the physiological response to hypoxia should lead to a greater understanding of the pathogenesis of HAPE and perhaps in the identification of new therapies.

Chronic hypoxia results in both structural changes in the pulmonary artery and a sustained increase in pulmonary vascular tone. This study investigated the effects of subacute moderate hypoxia on expression and function of potassium (K+) channels in rat pulmonary artery myocytes (PASMCs). The rats were kept at 0.67 atmospheres for 6, 12, or 24 h. We found that the expression of mRNA for voltage-activated K+ channels (Kv)1.2, Kv1.5, and Kv2.1 is reduced after less than 24 h of this moderate hypoxia. K+ current (Ik) is significantly inhibited in PASMCs from rats hypoxic for 24 h, resting membrane potential is depolarized and cytosolic [Ca2+] is increased in these cells. In addition, antibodies to Kv1.2, Kv1.5, and Kv2.1 inhibit Ik, cause membrane depolarization and attenuate both hypoxia- and 4-AP-induced elevation in [Ca2+]i in PASMCs from normoxic rats but not from 24 h hypoxic rats. Subacute hypoxia does not completely remove the mRNA for Kv1.2, Kv1.5, and Kv2.1, but antibodies against these channels no longer alter Ik or cytosolic calcium, suggesting that subacute hypoxia may inactivate the channels as well as reduce expression. As the expression of mRNA for Kv1.2, Kv1.5, and Kv2.1 is sensitive to subacute hypoxia and decreased expression/function of these channels has physiologic effects on membrane potential and cytosolic calcium, it seems likely that these Kv channels may also be involved in the mechanism of high-altitude pulmonary edema and possibly in the signaling of chronic hypoxic pulmonary hypertension.

Actually, it doesn't even do that.

Actually, it doesn't even do that.

Actually, it does do that. UIAA study claims Diamox helps the body to acclimatise to the lack of oxygen.
http://www.mountaineering.ie/...A03-DiamoxEtc(1).pdf

Sorry, that isn't a study. It's an old opinion piece by one doctor. You are confusing reducing the symptoms of AMS with actual acclimatization. It's an important distinction because even though you may not feel too bad it doesn't mean you are ready to go much higher. There are many aspects of acclimatization but the production of red blood cells is among the most important, for which acetazolamide does nothing. Going to an altitude and staying, thanks to Diamox is one thing. Going there, feeling okay, and then pushing much higher can put you in a world of hurt...HAPE/HACE.

You are confusing reducing the symptoms of AMS with actual acclimatization. It's an important distinction because even though you may not feel too bad it doesn't mean you are ready to go much higher.

There are many aspects of acclimatization but the production of red blood cells is among the most important, for which acetazolamide does nothing.

Reasons NOT to take diamox:

IT MAKES BEER TASTE LIKE SH**, never a good price to pay.

If You fools spent HALF as much Time Acclimating as you spend jabbering about Diamox, well....you wouldn't NEED ANY.