To stop heart attacks, we need more CO2
A study on 32 million heart deaths in 27 countries shows extreme cold killed four to six times as many people as extreme heat. Since climate change makes our hottest days hotter and warms our winter nights, this will mean less heart failure in the future.
For every extra summer death due to heart failure, six lives will be saved in winter thanks to people who burn oil. Obviously it’s time to subsidize coal plants to save medical costs. Every dollar spent warming the world is an investment against heart failure. You know the drill.
Naturally in science communication, headlines and truth are 180 degrees apart.
Climate change could worsen heart deaths linked to extreme temperatures
By Cara Murez, HealthDay News
A new multinational analysis of 32 million heart-related deaths over the past 40 years found more occurred on days with severe temperatures, an issue that climate change could make even worse.
The investigators compared heart-related deaths on the hottest and the coldest 2.5% of days in 567 cities with those on days when temperatures were optimal.
For every 1,000 heart-related deaths, there were an additional 2.2 deaths on days with extreme heat. There were also 9.1 additional deaths on days with extreme cold, the findings showed.
Among people with heart failure, there were 2.6 additional deaths on extremely hot days and 12.8 on extremely cold days, the researchers reported.
Remember the old cannard that climate change warms up nights faster than days (thus wiping out the coldest extremes)? Just ask the IPCC — They told us there are less cold days now and it’s because of climate change:
Based on the AR5 and SREX, as well as recent literature (see Supplementary Material 3.SM), there is high confidence (very likely) that there has been an overall decrease in the number of cold days and nights and an overall increase in the number of warm days and nights at the global scale on land.
As a bonus we gain more warmth at the cold end than at the top — stable temperature save lives!
In particular, they identified that one-quarter of the land has experienced an intensification of hot extremes (maximum temperature on the hottest day of the year, TXx) by more than 1°C and a reduction in the intensity of cold extremes by at least 2.5°C (minimum temperature on the coldest night of the year, TNn).
–IPCC. Chapter 3, SR15, 3.3.2.1
This was reported ad nauseum for the last twenty years, by NewScientist, unSkepticalScience, The Conversation, PopScience, the New York Times, and those scientific giants –The WEF (among a hundred thousand others). It was a defining feature, a fingerprint, of man-made climate change. It’s therefore obvious that climate change is a cardiac winner, and all the journalists know it.
It’s more evidence that Science Communication is not a profession but just a marketing exercise. Apparently, they’re not there to inform the public, just to scare tax dollars out of them.
So climate change causes colder winters now?
The medical paper simply says so:
Climate change produces both hotter summers and colder winters, rendering populations not accustomed to these unusual weather conditions vulnerable, especially in low-income areas where there may be less adaptability to changing conditions.
It’s not climate change that is deadly but climate change action. The more money we waste on unreliable energy the more people we kill from unaffordable energy bills.
Despite the paper having 51 references there were none to back up their “colder winters” claim.
The biology of hot and cold deaths:
To spare you the details, essentially heat causes dehydration and thickens blood, and is thus solvable with a glass of water. Cold causes vasoconstriction and high blood pressure, which is bad for everything, and solvable with fossil fuels.
There are some postulated underlying mechanisms that could explain the CVD mortality risk associated with extreme temperatures. Both cold and heat exposures evoke a series of synchronized autonomic and cardiovascular responses that ensures core body thermal homeostasis. Those responses are often altered and exaggerated with aging and in individuals with preexisting cardiovascular risk factors, leading to CVD events. Heat exposure leads to increased skin blood flow which dissipates heat, as well as increased sweating which evaporates heat. This leads to potential volume depletion and sympathetic system activation, resulting in increased heart rate and inotropy to maintain stroke volume despite decreased preload. Rising core body temperature also increases metabolic state and oxygen consumption. In susceptible individuals, these cascades may lead to demand ischemia or plaque rupture. Volume depletion and insensible body water losses leads to hemoconcentration and hypercoagulable states further increasing the risk of thrombosis and myocardial ischemia. Fluid shifts can disturb electrolyte balance (specifically, potassium, magnesium), increasing risk of arrhythmias in susceptible individuals. In patients with heart failure who receive diuretics, heat may result in severe volume depletion and potentially, shock.
On the other hand, cold exposure leads to increased sympathetic activity that vasoconstricts skin and increases skeletal muscle tone to generate and conserve heat. This leads to catecholamine-driven rise in blood pressure (mainly through an increase in peripheral vascular resistant), and hence, increased cardiac oxygen demand to overcome this increase in afterload. Cold also leads to increased cholesterol crystals deposition in atherosclerotic plaques, rendering susceptible individuals to plaque rupture and myocardial infarction. Last, hypothermia is known to induce hypercoagulability because of increased viscosity and hemoconcentration from fluid shifting into extravascular space and clotting factor abnormalities.
For extreme heat, get Gatorade. For extreme cold, move into Parliament.
Heart icon: PngFolio
REFERENCE
Alahmad Barrak et al (2022) Associations Between Extreme Temperatures and Cardiovascular Cause-Specific Mortality: Results From 27 Countries, Circulation, https://doi.org/10.1161/CIRCULATIONAHA.122.061832 2022;0