Individual Comprehensive Lab Report (Report Type R-3: Fill & Download for Free

First and foremost, it is really important to know that as of today (February 17, 2020), there is still much we do not know about SARS-CoV-2 (i.e. the official name of the novel coronavirus) and COVID-19 (i.e. the official name of the disease caused by SARS-CoV-2). This uncertainty makes this question difficult to answer with a short or simple response.However, epidemiologists and scientists from around the world are making rapid and significant real-time progress in understanding the nature of this novel coronavirus. Earlier today, a comprehensive report[1][1][1][1][2][2][2][2] from the China CDC was released on over 70,000 individual cases in China, which included data for 99% of confirmed cases globally as of February 11th, 2020.There is very little doubt that COVID-19 is dangerous, but just how dangerous requires a much deeper dive. Here were some of the key takeaways from this report and other research I have done on the topic.(1) COVID-19 is highly contagiousA main finding of this characterization and exploratory analysis of the first 72,314 cases of COVID-19 found in China in the 40 days between first recognition of the outbreak of pneumonia with unknown etiology on December 31, 2019 to the end of the study period on February 11, 2020 is that this novel coronavirus is highly contagious. It has spread extremely rapidly from a single city to the entire country within only about 30 days. Moreover, it has achieved such far-reaching effects even in the face of extreme response measures including the complete shutdown and isolation of whole cities, cancellation of Chinese New Year celebrations, prohibition of attendance at school and work, massive mobilization of health and public health personnel as well as military medical units, and rapid construction of entire hospitals.Let’s re-examine the COVID-19 timeline:Late December 2019: A cluster of pneumonia cases of unknown origin appears in Wuhan, the city now at the epicenter of this epidemic.December 31, 2019: Alert issued by the local Wuhan Municipal Health Commission to the China CDC and a notification was sent to the World Health Organization about this outbreak.January 7, 2020: The pathogen was identified as a new type of coronavirus, and given the name 2019-nCoV. It was now learned that this virus was closely related but distinct to the one that caused the SARS crisis in 2003.January 11, 2020: The first death is reported (person died two days earlier). The Wuhan Municipal Health Commission issues its first public report announcing this novel coronavirus[3] and starts issuing daily update reports.January 20, 2020: 7 confirmed patients have now died, the virus has spread outside of Wuhan, and this becomes a national issue. China’s National Health Commission takes over primary responsibility.January 23, 2020: China announces unprecedented quarantine operations in major cities ahead of the Lunar New Year holiday.In the roughly 1-month period following the first inkling that this might be more than just another flu outbreak, the number of cases went from 104 to +653 to +5,417 to +26,548 roughly every 10 days. In other words, every 240 hours, the number of cases was increasing between 5 to 8 times.This is retrospective data — after confirming cases through nucleic acid testing, individual cases were interviewed to determine (by examining symptoms or history of contact with known infected) the approximate date when they likely contracted the virus. It provides the most accurate view of how quickly this thing spread (note: this data does not provide an accurate view of total number of actual infections — confirmed cases very likely only represent a small fraction of total infections).There is an epidemiological term called R-naught (or R0) that measures the relative contagiousness of an infection. While I have not yet seen any re-calculations based on this new and comprehensive dataset, previous calculations have placed it in the same range as SARS but lower than measles[4][4][4][4].That is to say, it is highly contagious. But before panicking, let’s take a deeper dive into some of its other important characteristics.(2) COVID-19 disproportionately affects older people (and those with pre-existing medical conditions)Detailed demographic data was released in the China CDC report, which confirmed analysis from earlier reports[5][5][5][5][6][6][6][6][7][7][7][7](based on much smaller samples) as well as reports from outside of China (Hong Kong[8][8][8][8] and Singapore[9][9][9][9]) that older people are disproportionately impacted by COVID-19.1/ Summary information from various early in-depth case studies compared with overall numbers from Hubei, China ex-Hubei, HK, Singapore, Japan and the U.S. #COVID19 pic.twitter.com/zlVtAiJxak— Glenn Luk (@GlennLuk) February 16, 2020First, it appears that younger people have much more resistance to SARS-CoV-2 taking hold in their bodies when they are exposed to the virus. For example, patients under the age of 20 comprised only 2% of the confirmed cases (note: some of this may be due to adverse selection bias, which I will discuss in the next takeaway).Second, once younger people are infected with the virus, survival rates are higher. As of February 11th, there has only been a single person (out of nearly a thousand cases) under the age of 20 that is confirmed to have died from COVID-19.Meanwhile, the case fatality rate increases exponentially with each successive decade after the age of 40. Based on these reported case fatality rates, if you are over the age of 80, you are 69x more likely to die than someone under the age of 40.Pre-existing conditions (especially cardiovascular diseases and diabetes) have a similar impact and have likely played a role in the death of many of the relatively younger cases. And of course as you get older, there tends to be greater prevalence of pre-existing conditions — the two are related.These exponential leaps in mortality rates by age (and existence of pre-existing conditions) are very much in line with recorded death rates from general pneumonia[10][10][10][10] and seasonal flu, which makes complete sense because pneumonia — an infection of the lungs that causes inflammation of the lung — is what is causing the vast majority of COVID-19 fatalities.Even at this early stage where there are still a lot of unknowns, I would highly recommend that older people or those with pre-existing conditions stay extra vigilant and heed recommendations from WHO and other authorities.(3) Case Fatality Rate and importance of contextWhen confronted with something new like COVID-19, it is natural for many people to look to past epidemics as a basis for comparison. The most common ones that COVID-19 has been compared with are — by rough order of severity / global impact:Regular flu (seasonal)SARS[11] (2003)MERS[12] (2015)Swine Flu Pandemic[13] (2009)1918 Influenza Pandemic[14]With these epidemics, on top of the R0 number mentioned earlier measuring contagiousness, the other number people latch onto is Case Fatality Rate (CFR), or the number of deaths per number infected (at least those that can be counted). A common chart I have seen is this:Source: NY TimesOn the one hand, you have seasonal flu which has an estimated CFR in the 0.10–0.14% range[15][15][15][15][16][16][16][16]. Then you have MERS with a CFR of over 30%[17][17][17][17] which is justifiably scary.Currently the numbers based on confirmed COVID-19 cases in China are at 2.6% (as of February 17, 2020). 1,868 people have died out of 72,436 confirmed cases[18][18][18][18].A natural instinct is to take this 2.6% number, multiply by an estimated number of infections, and figure out what the potential death totals may be. And based on the “highly contagious” nature of the disease — with credible experts estimating potential infection rates of 40-70% of global population[19][19][19][19] — you arrive at some massive, panic-worthy numbers, fast.But that is why context is so important. Once we start talking about total infections, 2.6% is likely the upper bound, and possibly too high by one or even two orders of magnitude. To understand why, we need to understand what the confirmed number actually represents.The China CDC report provides an in-depth description of the process by which infections are confirmed. Originally, cases were only confirmed if a nucleic acid test on a throat swab sample came up positive. However, as the report describes, the procedure is “slow, labor intensive, and requires specialized equipment and skilled technicians”.Given this was a new viral strain, and especially at the early stages of the crisis, there was limited capacity in how many lab tests could be done properly (and safely) every day.9b/ For example, the report cites how nucleic acid testing is "slow, labor intensive, and requires specialized equipment and skilled technicians" as the unfortunate passengers on the Diamond Princess cruise liner recently experienced https://t.co/YRbM9qJQeV pic.twitter.com/bFFelG9B6M— Glenn Luk (@GlennLuk) February 18, 2020Meanwhile, in Wuhan, the epicenter of the epidemic, local hospital and medical resources were hit hard by the sudden surge in cases. Not only were there limits on testing capacity, healthcare workers on the frontlines were contracting the virus (and likely passing it on to patients and each other): the China CDC report confirmed that 1,716 health workers were lab-confirmed with COVID-19, and 87% of these were in Wuhan or Hubei Province[20][20][20][20].In other words, there was tremendous strain on local medical resources in Wuhan to not only diagnose and test patients, but to quarantine and care for sick patients as well. There are plenty of verified anecdotes that confirm that sick patients had to be turned away due to lack of capacity, including a prominent director and some of his immediate family members[21][21][21][21] that were forced to self-quarantine.This means that the cases that were confirmed and accepted into the overloaded local medical system were adversely selected for the most serious cases. And with the system under so much stress, there weren’t enough resources (both people and equipment) to care for those in the most critical condition — which invariably led to even higher mortality rates.Update (2/18): Mike Ryan, Executive Director at the World Health Organization re-iterated these points at WHO’s most recent press conference[22][22][22][22](emphasis mine):“… Remember at the beginning of the outbreak, what people were finding were the severe cases, so you have a huge bias at the beginning of the outbreak because what you find are the really sick people coming forward. And now we are going out looking for the less sick people …… so you can have a … false sense of mortality at the beginning and we saw that … in the pandemic of H1N1 … we saw fatality rates of 10 and 20% in the beginning because only the severe cases were presenting and a few weeks later the pattern was entirely different.”“There’s also the fact that the case fatality is different inside Hubei and Wuhan to the other provinces. And that may also reflect the fact that the pressure on the system in Wuhan and Hubei has been so severe and the lessons that have been learned … are being applied elsewhere and people are getting into earlier critical care.One of the issues has been predicting patients who have the co-morbidities and underlying conditions and ensuring they are transitioned into the critical care or severe care pathway early and that we’re not blocking up the system with the mild cases. And I think the system in China … has gotten much better at prioritizing those more likely to be severely ill into the system.It’s also very difficult in critical care to ventilate so many patients and do ECMO[23][23][23][23] with so many patients. It takes quite a lot of technical skill. It’s not just the machinery, it’s the technicans who use that. And again, bringing them up to speed, bringing in the emergency medical teams … remember 127 emergency medical teams, nearly 10,000 specialist medical workers were sent into Hubei from outside. Pre-trained, pre-certified medical teams who were used to mass casualty management. They would have helped to reduce case fatality.So what we are seeing is a mixture of the fatality reducing probably because of better and better interventions over time but also because we’re finding more mild cases.”So 2.6% is not a number that you can apply to the broad infected pool. A better way to think about it is as the mortality rate for an adversely selected pool of cases that is on balance significantly older and sicker than the general population.Indeed, this adverse selection effect was demonstrated during the recent Swine Flu epidemic. As epidemiologists collected case information on the ground in the middle of the crisis, initial CFRs were calculated in the ~10% range[24][24][24][24]. However, once researchers had time to properly estimate infection rates in the population (e.g. by looking for the presence of specific antibodies in blood), they realized that vast swathes of the population had gotten infected but had not exhibited serious enough symptoms to be counted — and the effective mortality rate plunged two orders-of-magnitude lower to ~0.1%.(4) The situation in Wuhan is very bad. But it may also (hopefully) be unique.We can see just how different Hubei’s predicament looks from the rest of China, which had the benefit of greater awareness, the implementation of quarantines to slow the spread of infection, and less strain on local medical resources to identify and care for new confirmed cases. The differences in outcomes are about as clear as can be:As we can see here, the mortality rate is significantly lower outside of Hubei, at 0.6%. The ratio of patients that have been cured and discharged to those who have died is almost 60:1.Among patients that have yet to be discharged, the China CDC report encouragingly reported that “no deaths have occurred among those with mild or even severe symptoms”. Singapore’s Ministry of Health also indepedently reports that patients that are still hospitalized are “in stable or improving” condition and highly likely to survive[25][25][25][25].Furthermore, the demographic information from cases outside of China (e.g. Singapore and Hong Kong) also show ratios that are more inline with China ex-Hubei than Hubei itself.Indeed, the key lesson here may be that controlling this thing before it can get to such a critical mass that it overwhelms the local medical system and resources is extremely important.And hopefully there is some light at the end of tunnel for Wuhan as it appears that officials are making progress working through some of the city’s capacity issues:1/ #COVID19 Key tidbit here is that Wuhan is finally ramping up capacity to take on patients with "mild symptoms", which in the past have had to be turned away due to lack of capacity. Here is some further context around these numbers. https://t.co/NIDlMNev5S— Glenn Luk (@GlennLuk) February 17, 2020ConclusionAs I stated at the very beginning, there are still many unknowns out there. That is why there is no simple answer to the question of how dangerous this thing really is. Among others:There is no vaccine against COVID-19 (one that can be deployed safely at scale)We are still unsure about how contagious this is in people that are infected but asymptomaticWe do not know how many people are infected, because (very likely) many people are infected and not yet identified for a variety of reasonsWe do not know exactly why infection and/or mortality rates for young people are so much lowerWe do not know how countries with less-developed healthcare systems will be able to cope with potential outbreaksSARS-CoV-2 will continue to mutate and evolve (although scientists aren’t that worried about this[26])It’s hard to predict the second-order effects (e.g. policy under/over-reaction, economic disruption, etc.)To make matters worse, with so much uncertainty on a topic that is highly technical and specialized — amplified by modern social media platforms which tend to reward simple and extreme vs. complex and nuanced — there is also a significant amount of misinformation out there. As discussed on a recent NPR podcast[27][27][27][27] with Carl Bergstrom, professor at the University of Washington that studies the spread of scientific disinformation:FADEL: What are the myths that are out there? Let's start there.BERGSTROM: Well, there's a wide range of different stories that are out there. They range from misinformation about - simply about the rate at which the disease is spreading, misinformation about how many people it's killing. And then you get some really wild stuff out there like stories that it might have been a bio-weapon - it is not - sort of anything that could capture the imagination, get people scared, get people to spread them further.FADEL: So what's behind all this disinformation, this misinformation? What's behind it?BERGSTROM: This is a really fascinating case because there are a whole bunch of different sources of misinformation, and they have a whole bunch of different motives. Disingenuous actors - they want to spread misinformation to make China look as bad as possible and decrease trust of people within China for their own government and decrease trust from people outside of China for the Chinese government. They could potentially lead to various kinds of disruptions of, you know, normal international relations or normal international commerce and so forth.FADEL: Right.BERGSTROM: Then you get people that are simply spreading misinformation for profit, using this to sell, you know, snake oil treatments of various kinds. And then finally, there are a lot of well-meaning people that are scared and are not able to get good information and are sharing that because they're trying to take care of their friends and family, which is a very natural human emotion, of course.FADEL: Why does this misinformation spread so quickly?BERGSTROM: One of the things that's making the misinformation spread so quickly in this particular case is that there's a information vacuum. There's a ton of uncertainty surrounding what's actually going on with this virus. People are looking for answers that provide certainty. Most experts are unwilling to give answers like that because we simply don't know. I can give you a very broad range of how infectious the disease might be, how many people it might reach, how likely it is to kill you. But I can't give you a sharp number.What people really want to hear are these sharp numbers, and if someone makes them up and states them in ways that seem authoritative, those are the kinds of pieces of misinformation that are likely to go spreading rapidly across social media.All of this disinformation and noise leads to an entire spectrum of human emotional response from denial and anger to fear and outright panic. But excessive over-optimism or fear can both lead to sub-optimal outcomes. Over-optimism can lead to under-estimating or ignoring the potential risks. Panic can lead to “medicine” that harms the patient more than the disease itself.And sadly, fear and anger have given way to xenophobia and racism[28][28][28][28], bringing out some of the worst of human nature.At this point, the most important thing for us as a global society is to problem-solve together to clear as many of these unknowns as possible, as fast as possible. The public release of this comprehensive dataset and associated analysis is one big step to this end goal. But there is a lot more work to be done until we defeat this thing, not to mention codifying the lessons learnt so that we are better prepared to deal with the next one.Footnotes[1] https://github.com/cmrivers/ncov/blob/master/COVID-19.pdf[1] https://github.com/cmrivers/ncov/blob/master/COVID-19.pdf[1] https://github.com/cmrivers/ncov/blob/master/COVID-19.pdf[1] https://github.com/cmrivers/ncov/blob/master/COVID-19.pdf[2] http://weekly.chinacdc.cn/fileCCDCW/journal/article/ccdcw/newcreate/COVID-19.pdf[2] http://weekly.chinacdc.cn/fileCCDCW/journal/article/ccdcw/newcreate/COVID-19.pdf[2] http://weekly.chinacdc.cn/fileCCDCW/journal/article/ccdcw/newcreate/COVID-19.pdf[2] http://weekly.chinacdc.cn/fileCCDCW/journal/article/ccdcw/newcreate/COVID-19.pdf[3] http://www.nhc.gov.cn/xcs/yqtb/202001/1beb46f061704372b7ca41ef3e682229.shtml[4] The Deceptively Simple Number Sparking Coronavirus Fears[4] The Deceptively Simple Number Sparking Coronavirus Fears[4] The Deceptively Simple Number Sparking Coronavirus Fears[4] The Deceptively Simple Number Sparking Coronavirus Fears[5] Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China[5] Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China[5] Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China[5] Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China[6] Clinical Characteristics of Patients With 2019 Novel Coronavirus (2019-nCoV)–Infected Pneumonia in Wuhan, China[6] Clinical Characteristics of Patients With 2019 Novel Coronavirus (2019-nCoV)–Infected Pneumonia in Wuhan, China[6] Clinical Characteristics of Patients With 2019 Novel Coronavirus (2019-nCoV)–Infected Pneumonia in Wuhan, China[6] Clinical Characteristics of Patients With 2019 Novel Coronavirus (2019-nCoV)–Infected Pneumonia in Wuhan, China[7] Clinical Characteristics of Patients With Novel Coronavirus (2019-nCoV) Infection Hospitalized in Beijing, China[7] Clinical Characteristics of Patients With Novel Coronavirus (2019-nCoV) Infection Hospitalized in Beijing, China[7] Clinical Characteristics of Patients With Novel Coronavirus (2019-nCoV) Infection Hospitalized in Beijing, China[7] Clinical Characteristics of Patients With Novel Coronavirus (2019-nCoV) Infection Hospitalized in Beijing, China[8] https://www.chp.gov.hk/files/pdf/enhanced_sur_pneumonia_wuhan_eng.pdf[8] https://www.chp.gov.hk/files/pdf/enhanced_sur_pneumonia_wuhan_eng.pdf[8] https://www.chp.gov.hk/files/pdf/enhanced_sur_pneumonia_wuhan_eng.pdf[8] https://www.chp.gov.hk/files/pdf/enhanced_sur_pneumonia_wuhan_eng.pdf[9] Updates on COVID-19 (Coronavirus Disease 2019) Local Situation[9] Updates on COVID-19 (Coronavirus Disease 2019) Local Situation[9] Updates on COVID-19 (Coronavirus Disease 2019) Local Situation[9] Updates on COVID-19 (Coronavirus Disease 2019) Local Situation[10] Can You Die from Pneumonia? What You Need to Know[10] Can You Die from Pneumonia? What You Need to Know[10] Can You Die from Pneumonia? What You Need to Know[10] Can You Die from Pneumonia? What You Need to Know[11] Severe acute respiratory syndrome - Wikipedia[12] Middle East respiratory syndrome - Wikipedia[13] 2009 flu pandemic - Wikipedia[14] Spanish flu - Wikipedia[15] Burden of Influenza[15] Burden of Influenza[15] Burden of Influenza[15] Burden of Influenza[16] Estimated Influenza Illnesses, Medical visits, Hospitalizations, and Deaths in the United States - 2017-2018 influenza season[16] Estimated Influenza Illnesses, Medical visits, Hospitalizations, and Deaths in the United States - 2017-2018 influenza season[16] Estimated Influenza Illnesses, Medical visits, Hospitalizations, and Deaths in the United States - 2017-2018 influenza season[16] Estimated Influenza Illnesses, Medical visits, Hospitalizations, and Deaths in the United States - 2017-2018 influenza season[17] Middle East respiratory syndrome coronavirus (MERS-CoV)[17] Middle East respiratory syndrome coronavirus (MERS-CoV)[17] Middle East respiratory syndrome coronavirus (MERS-CoV)[17] Middle East respiratory syndrome coronavirus (MERS-CoV)[18] http://www.nhc.gov.cn/xcs/yqtb/202002/261f72a74be14c4db6e1b582133cf4b7.shtml[18] http://www.nhc.gov.cn/xcs/yqtb/202002/261f72a74be14c4db6e1b582133cf4b7.shtml[18] http://www.nhc.gov.cn/xcs/yqtb/202002/261f72a74be14c4db6e1b582133cf4b7.shtml[18] http://www.nhc.gov.cn/xcs/yqtb/202002/261f72a74be14c4db6e1b582133cf4b7.shtml[19] Expert Opinions on the COVID-19 coronavirus outbreak[19] Expert Opinions on the COVID-19 coronavirus outbreak[19] Expert Opinions on the COVID-19 coronavirus outbreak[19] Expert Opinions on the COVID-19 coronavirus outbreak[20] UPDATE 1-China says 1,716 health workers infected by coronavirus, six dead[20] UPDATE 1-China says 1,716 health workers infected by coronavirus, six dead[20] UPDATE 1-China says 1,716 health workers infected by coronavirus, six dead[20] UPDATE 1-China says 1,716 health workers infected by coronavirus, six dead[21] Four Deaths in One Family Show Danger of Wuhan’s Home Quarantine Policy[21] Four Deaths in One Family Show Danger of Wuhan’s Home Quarantine Policy[21] Four Deaths in One Family Show Danger of Wuhan’s Home Quarantine Policy[21] Four Deaths in One Family Show Danger of Wuhan’s Home Quarantine Policy[22] Who @WHO[22] Who @WHO[22] Who @WHO[22] Who @WHO[23] https://www.thoracic.org/patients/patient-resources/resources/what-is-ecmo.pdf[23] https://www.thoracic.org/patients/patient-resources/resources/what-is-ecmo.pdf[23] https://www.thoracic.org/patients/patient-resources/resources/what-is-ecmo.pdf[23] https://www.thoracic.org/patients/patient-resources/resources/what-is-ecmo.pdf[24] How deadly is the new coronavirus? Scientists race to find the answer[24] How deadly is the new coronavirus? Scientists race to find the answer[24] How deadly is the new coronavirus? Scientists race to find the answer[24] How deadly is the new coronavirus? Scientists race to find the answer[25] MOH | News Highlights[25] MOH | News Highlights[25] MOH | News Highlights[25] MOH | News Highlights[26] Mutation, Adaptation, and Virus Genomes – A Primer for the Public[27] Troll Watch: Misinformation Around The Coronavirus[27] Troll Watch: Misinformation Around The Coronavirus[27] Troll Watch: Misinformation Around The Coronavirus[27] Troll Watch: Misinformation Around The Coronavirus[28] Xenophobia and racism related to the 2019–20 Wuhan coronavirus outbreak - Wikipedia[28] Xenophobia and racism related to the 2019–20 Wuhan coronavirus outbreak - Wikipedia[28] Xenophobia and racism related to the 2019–20 Wuhan coronavirus outbreak - Wikipedia[28] Xenophobia and racism related to the 2019–20 Wuhan coronavirus outbreak - Wikipedia

We don't know.We won't have long-term data until there has been 20 years of vaping*, which will be in 2025. The indications, from examination of the ingredients, are that inhalation of these materials, heated mildly in a nebulising process, should have little clinical significance.* Vaping (see Oxford Dictionary): the action of using an electric or electronic vaporiser, with a nebulising process, to consume a flavoured liquid refill normally containing nicotine, as an alternative to smoking or a way of avoiding or ceasing smoking.There are of course a number of issues:- The individual ingredients are all approved for consumption in medicines, with the exception of those flavourings that do not have pharmaceutical licences for inhalation (food flavours). In some cases they have been inhaled without significant issues for 70 years (i.e. PG, propylene glycol, one of the excipients).- There is always a possibility that ingredients are harmless by themselves, but when combined with others they may produce other materials with undesirable qualities. This has not been noted to date.- Vaping is not a homogenous activity:(1) There are tens of thousands of products, and quite literally millions of combinations. For example, one retailer alone has over 7,000 refill products for sale, when all the possible combinations they sell of base, flavour and strength are totalled up. Then multiply this by the thousands of hardware combinations (ecig variants plus heads) and a total of over a million variations is easily reached. Even a 20-minute search on the web will give you many thousands of possible combinations.(2) Vaping has now split into a 2-tier activity - M2L vapers and D2L vapers.- Mouth-to-lung inhalers first draw into the mouth, then inhale. These vapers tend to use high resistance atomisers of over 1.5 ohms that produce average vapour volume (obviously, there is a limitation imposed by the maximum volume of the preliminary mouth draw). Their daily refill consumption seems to average 3 or 4ml, with a range from 1.5ml to 8ml.- Direct-to-lung vapers tend to use low-resistance atomisers around 0.5 ohms or lower, and create very high vapour volume; the volume is governed by the full lung capacity since they inhale direct to the lung. These vapers report daily usage of 15ml and upward, with 30ml daily consumption reported on occasion.- Then, there are also puffers who vape like pipe smokers, without any great lung involvement.It is probably impossible that any implications for the lungs would be the same for all groups.OpinionsDr Laugesen was the first researcher, many years ago, to point out that it is impossible for vaping to cause lung cancer, as none of the carcinogenic materials or operators are present: there is no smoke. There are some residual TSNAs in the nicotine, but at the same quantities as present in pharmaceuticals since both products use pharma-grade nicotine base. This quantity, typically 8ng/gm, is insignificant and irrelevant.The CEO of ASH UK stated at a conference of American doctors, "E-cigarettes are unlikely to ever kill anyone". ASH are an anti-smoking lobby group and so are hardly likely to underestimate any harm from these types of activities. Even I would not be so bold as to make such a statement, and I cannot see anything likely to be implicated in any serious health outcomes associated with ecig use. However, there is always going to be a strong possibility that a smoker with lungs seriously compromised by smoking, such as an emphysema patient, may contract pneumonia after switching to vaping, since emphysema patients regularly get pneumonia and die as a result. If they happen to be vaping, then this will be implicated, rightly or wrongly.Your itemised concernsTo address your list of concerns: the long-term health impact is unknown. Compared to smoking, we could reasonably estimate a 1,000 times reduction in those toxins still present, and the elimination of many of the most serious since there is no tobacco and no smoke. Therefore a risk reduction of 3 or even 4 orders of magnitude seems likely.Flavourings: while some flavours such as menthol have pharmaceutical licenses for inhalation, the vast majority don't. This area is indeed where most of the issues are likely to be found. At present we know some flavours can be irritants, and some may be toxic - but no one knows what doses are needed for negative health impact. The flavour most likely to have implications is said to be diacetyl, but there again it is present in tobacco smoke at much higher levels (20 - 100x) and no one has ever, to my knowledge, diagnosed in smokers the lung disease specifically generated by this flavouring (bronchiolitis obliterans or 'popcorn lung'). Since it only takes a short time to present in those exposed to high levels of diacetyl (typically 4 years), and a comparatively short time in those exposed to low levels (10 years), we should expect to have already seen some cases in vapers if this is going to be an issue - [at 2017] there are more than 30 million vapers globally; we have 12 years’ product experience; and over 100 million user-years in total. Compare this with an average 40 years' smoking for peak presentations of serious lung disease in smokers (the age 70 decade is the peak presentation epoch for serious lung disease in smokers, indicating at least a 40-year timelag after smoking initiation). Since we do not see any popcorn lung in smokers, who inhale diacetyl in much higher quantities than vapers do ( the pathology is unmistakeable and therefore it would be noted), and since we have no cases among vapers even with sufficient time having elapsed, and since we have 100 million user-years plus without any presentations, it could be that this issue is not of great significance. Even if we see 5 cases per 10 years, globally, an incidence of 5 cases in 20 or 30 million would not normally be considered of any relevance since such a low rate of occurrence could easily be due to confounders of some kind.Where to buy flavours: for maximum risk reduction, a DIY vaper might buy materials from suppliers who can present an independent lab test certificate. Suppliers such as FlavourArt have a considerable investment in safety procedures and testing. The market leaders in independent analysis and safety testing in this area are Enthalpy, Inc.Health impact: the general consensus from (literally) millions of posts on the major forums is that health improvements are significant after switching from smoking to vaping. This appears to also include those with conditions such as diabetes and thyroid problems, who do not see any negatives. In some cases where we would expect to see improvements in smokers who totally quit - for example, in diabetes, high blood pressure, and early stage COPD - those improvements are also seen in vapers previously with those conditions. Prof Polosa, the pulmonary specialist, shows cases where harm reversal has occurred.I have assembled the most comprehensive list of smoking cessation symptoms that exists, to my knowledge, including implications for thyroid patients and similar; viewed in the context of a switch to vaping. It can be found here:A list of symptoms when quitting tobacco and changing to an ecigaretteThe main issue here is that smoking cessation can lead to a range of symptoms that people seem in general to be unaware of. In fact, it is even possible to find statements on the internet such as, "There are no negative consequences to smoking cessation", which you will see is incorrect.Doctor's opinions: there are doctors, and then there are doctors. Doctors are just as vulnerable to propaganda as anyone else. This was revealed rather clearly by a recent survey that revealed 44% of British doctors thought nicotine caused cancer. This is hilariously wrong, since nicotine has no association with cancer, and their official clinical guidance makes this very clear: NICE PH45. So as with anything else, you have to choose your 'expert' carefully. Luckily there are plenty of good resources, including quotes by *all* of the senior public health figures in the UK, and most of the highest regarded public health experts in the world; for example Prof JF Etter of Geneva and Prof John Britton of the RCP (and no one is going to argue with them unless they wish to look very, very stupid).Britton says: "If all the smokers in the UK switched to ecigs, we would save five million lives just among those alive today in the UK". Similarly, Prof R West says, "E-cigarettes are probably about as safe as drinking coffee". West produces the world's most up to date, accurate, current and honest smoking and vaping statistics, in his longitudinal study The Smoking Toolkit, produced along with YouGov and ASH. He shows very clearly that [at mid-2017]:More than half of vapers have quit smokingThere is no significant number of non-smokers or youths using ecigsThere is no gateway from vaping to smoking: it is an off-rampVaping is now the most successful method for smoking cessationFear-mongering: the world's largest and most expensive propaganda campaign is being conducted in this space, to try and protect cigarettes sales. Enormous tax revenues, pharmaceutical sales and cigarette sales are at stake. Just one pressure group, Legacy in the USA (now renamed Truth Initiative, presumably with unconscious irony and no knowledge of Orwell etc.) has an annual income of hundreds of millions of dollars. The funds available for propaganda are truly stratospheric.All vaping will do is destroy these vast revenues - the world's largest gravy train - without providing much at all except a tremendous public health gain unseen since the invention of antibiotics. You can't tax something that doesn't kill anyone, and you can't make billions in drug sales treating people who don't get ill. THR (Tobacco Harm Reduction) is an economic time bomb in the making, and the people making the fortunes are desperate to stop the Swedish Miracle spreading.Sweden has unique national health statistics, as half of tobacco consumers there don't smoke, they use Snus, and therefore smoking is disappearing along with all the morbidity, mortality, huge taxes, and vast profits - at zero cost to the state (that's why it's called the Swedish Miracle). Sweden has the lowest tobacco-related mortality of any Western developed country by a wide margin; and everyone who counts is working as hard as possible to make sure that doesn't happen in any other country. Hence, the propaganda.Slovenian doctors: if vapers needed lung transplants after 5 years, then we'd already have had around 10 million deaths or lung transplants. So much for that. We haven't seen one, never mind ten million.I suggest it is more sensible to listen to Prof Etter or Prof Britton, who are the world's most senior tobacco control figures. Britton is the Chair of the Royal College of Physicians, Tobacco Group. The RCP is about 500 years old and almost certainly the most conservative organisation in the world; they probably think of aspirin as a radical new therapy to be viewed with suspicion. If they support ecigs wholeheartedly, you have to wonder about the mental midgets who want to protect cigarette sales (or perhaps more relevant: who is paying them). When you look at who argues against vaping as a substitute for smoking, you can always and without exception find a money trail leading back to those who profit from smoking, often in the pharmaceutical industry or among those who gain from MSA funding and the like. As one spokesperson from a public health organisation who refused to take the money reported, "We have had numerous offers from the pharmaceutical industry to lobby against e-cigarettes".Particulates: I am reliably informed by professors of particulates (actually, the professors of biochemistry, physics, and occupational health science who make the regulations for occupational exposures) that smoke and vapour are different. To put it simply, smoke is a solids-based aerosol and vapour is a liquid-based aerosol. Smoke particulates are deposited in the lungs; some of the material remains on the lung surface and some passes into the bloodstream, where a percentage is of a harmful nature. Liquid aerosols are absorbed, dispersed and excreted by the lungs, as this is a basic function of the lung. The impact is very similar to that experienced in the countless trillions of hot, soapy showers people have taken, where billions of water and VOC particulates (from the soap) are inhaled in every single shower. Apparently there are no thousands or millions of cases of lung damage to be seen as a result of taking hot showers, and they say it is unlikely vaping will be any different. Go outside on a cold morning and exhale: you will now see the water vapour being expelled by the lungs, it is always there, and it is a natural function.The excipients in refill liquid are mainly PG and glycerol. PG has been inhaled for 70 years and has no clinical significance. It is the most common excipient (carrier, solvent) used in asthma inhalers, although it is gradually being replaced by glycerol (glycerine, VG). It is also the carrier in the inhaler therapies given to lung transplant patients. I believe it is reasonable to assume that if a material is the basic ingredient in medical inhalers, has been used as such for decades, and can be given to those in the most fragile health and with the most delicate lung conditions, then there can be no substantive case for suggesting that if the same ingredient is sold as a consumer product then large numbers of lung transplants will be needed. In fact, a reasonable person would probably conclude this is complete lunacy. Or something more profitable.Corruption: how dare you suggest that governments and giant multinationals like money better than your health? This is tantamount to insurrection, and I hope you regret this dangerous thought.Some associated issues of interestResearchWe can now find over 1,000 separate studies on vaping and related issues, in a search. Every possible subject is represented, and there are multiple studies, CTs and RCTs on any aspect. Please remember a main principle of the scientific method: look at all the evidence, not just some of it; and not just the bit you happen to like. There is no paucity of ecig research; there is a plethora.If someone tells you, "But this study by Pharmapimp, Sockpuppet et al says there is so much formaldehyde in ecig vapour that Egyptian-type mummies are created by vaping for 3 days", then find the other 20 studies on the same thing and see what they say; find who paid for the study; and find what specialists said about the 'formaldehyde, mummies and vaping' study, perhaps here:E-cigarette ResearchNicotineIt is impossible to clinically demonstrate any potential for dependence on nicotine. In the multiple clinical trials where large quantities of pure nicotine were administered daily for several months to never-smokers, no person has ever shown any sign of dependence. See for example the work of Dr Paul Newhouse of Vanderbilt, the world authority. His day job is giving large amounts of nicotine to unexposed subjects, in the search for new therapies for neurodegenerative diseases and so forth. In his words, "The risk of addiction to nicotine alone is virtually nil."The risk of 'addiction' to nicotine for non-smokers taking up vaping is approximately zero. Nicotine dependence results from delivery with multiple potentiators and synergens especially in tobacco smoke, which cause a persistent change in brain chemistry. You could probably make many things 'addictive' if you could freely mix in another 9,600 compounds to get exactly the result you want (9,600 separate compounds have been identified in tobacco and tobacco smoke - Rodgman, Perfetti 2013).A good citizen will keep smoking, and keep paying those huge taxes. They will keep on smoking till they get profitably ill with something like diabetes or cancer. They will keep on smoking, or try and quit with pharmaceutical interventions, which helpfully have a 9 out of 10 failure rate, and therefore lead straight back to smoking. They will keep smoking until they die early. A good citizen will die at age 65, on the day they become eligible for their pension, thus saving the government a veritable fortune when the sum is multiplied up with all the others conveniently dying early.A sensible citizen might well consider a switch to vaping, and refuse to buy government tobacco ever again.Q: "What are the long-term health effects of e-cigarettes likely to be?"

You mention that he is an undiagnosed schizophrenic - yet you say he doesn’t take his meds every day. Has he been diagnosed or not?Why would you want to have a relationship with someone who is seriously mentally ill? Life with a mentally ill person is very unstable and unpredictable. In many cases they can’t hold down a job. Are you ready to support him financially for the rest of your life? Are you prepared to have children who might inherit their fathers disease?I have inserted below an article on Schizophrenia - please read it right to the end,Emotion in Schizophrenia: Where Feeling Meets ThinkingAnn M. Kring and Janelle M. CaponigroAuthor information Copyright and License information DisclaimerSee other articles in PMC that cite the published article.AbstractOur understanding of the nature of emotional difficulties in schizophrenia has been greatly enhanced by translational research over the past two decades. By incorporating methods and theories from affective science, researchers have been able to discover that people with schizophrenia exhibit very few outward displays of emotion but report experiencing strong feelings in the presence of emotionally evocative stimuli or events. Recent behavioral, psychophysiological, and brain imaging research has pointed to the importance of considering the time course of emotion in schizophrenia.This work has shown that people with schizophrenia have the ability to experience emotion in the moment; however, they appear to have difficulties when anticipating future pleasurable experiences, and this perhaps affects their motivation to have such experiences. While advancements in our understanding of emotional experience and expression in individuals with schizophrenia have been made, these developments have led to a new collection of research questions directed at understanding the time course of emotion in schizophrenia, including the role of memory and anticipation in motivated behavior, translating laboratory findings to the development of new assessment tools and new treatments targeting emotional impairments in people with this disorder.Keywords: schizophrenia, emotion, anticipation, memorySchizophrenia is a disorder that impacts many domains. Some of its more recognizable symptoms involve difficulties in thinking (e.g., disorganized thinking, delusions) and perception (e.g., hallucinations). While these symptoms may come and go with episodes, some of the more long-lasting symptoms involve difficulties in emotion. In particular, the so-called negative symptoms of flat affect (lack of outward expression of emotion), anhedonia (diminished experience of pleasure), and avolition (diminished motivation) all involve emotion.These symptoms are often resistant to medication and are associated with poor overall functioning, pointing to the importance of understanding emotion in schizophrenia.What do we mean by emotion? Most psychological researchers and theorists agree that emotions are responses to events, whether internal or external, that consist of multiple components including outward expression (e.g., a smile), reported experience (e.g., reporting feelings of happiness), physiology (e.g., increased heart rate), appraisal (e.g., labeling one’s experience and its probable cause), and brain activation (e.g., activation in certain areas of the prefrontal cortex).Kring (1999) summarized the state of the field with respect to understanding emotional difficulties in schizophrenia and pointed toward promising future directions. Ten years later, much of this promise has been realized, and exciting new avenues for the assessment and treatment of emotional difficulties in schizophrenia are now underway. In this paper, we review our current understanding of how emotion does (or does not) go awry among people with schizophrenia and then highlight the ways in which these research findings have been translated into current assessment and treatment strategies.Our understanding of the nature of emotional difficulties in schizophrenia has become much clearer in the last two decades because of translational research. Specifically, researchers have adopted the methods and theories developed in affective science and neuroscience to study emotion in schizophrenia. These methods include laboratory studies in which emotionally evocative stimuli are presented to people with and without schizophrenia and measures of facial expression, reported experience, physiology, and brain activation are obtained. A remarkably consistent pattern of findings has emerged from these studies (see Kring & Moran, 2008, for review): In the presence of emotionally evocative stimuli—whether they be films, pictures, foods, odors, or sounds—people with schizophrenia are less outwardly expressive of positive and negative emotion than are people without schizophrenia. However, people with schizophrenia report feeling emotions as strongly as, if not stronger than, people without schizophrenia. Additionally, studies of emotion in the context of daily life find the same pattern of results: People with schizophrenia experience strong feelings in their day-to-day lives even though the contexts in which they experience these feelings are different from those without the disorder.A Closer Look at Emotional ExperienceOver the past 10 years, researchers have taken a closer look at emotional experience in schizophrenia. Many question whether people with schizophrenia can complete a self-report rating scale about their feelings given concurrent problems with disorganized thinking that may accompany the disorder. However, people with schizophrenia draw upon the same knowledge structures of emotion when reporting on their experiences as do people without schizophrenia (Kring, Barrett, & Gard, 2003), bolstering our confidence in these reports of emotion experience. Further, reports of emotional experience are stable across time and medication status (Kring & Earnst, 1999). This is not to say that symptoms may not impact reports of emotional experience, in the same way that any type of context may influence people’s reports of emotional experience, regardless of whether an illness like schizophrenia is involved. Yet, the emotion reports of people with schizophrenia are just as reliable and valid as those of people without the disorder.Results of studies using physiological measures of emotion (e.g., skin conductance, facial muscle activity, startle modulation) support the findings of comparable reports of emotional experience between people with and without schizophrenia, thus rendering less likely the possibility that people with schizophrenia are reporting feelings according to the demands of the experimental situation. For example, an indirect physiological measure of emotional response is the magnitude of an eye blink in response to a startling noise. If a person is in a negative emotional state when hearing the startling noise, the blink response will be larger than it will be if the person is in a neutral state or a positive emotional state. Four studies have now shown that people with schizophrenia show the same pattern of blink response (or emotion-modulated startle) as do people without schizophrenia (Kring & Moran, 2008).Findings from brain activation studies using functional magnetic resonance imaging (fMRI) or positron emission tomography (PET) during the presentation of emotionally evocative stimuli are more mixed. Several studies have found that, compared to people without schizophrenia, those with the disorder show less activation of the amygdala (an area of the brain linked to the salience of stimuli, including emotional intensity) in response to positive and negative stimuli (see Aleman & Kahn, 2005, for review), but other studies find comparable or even greater amygdala activation among people with schizophrenia; some studies have found decreased activation in areas of the prefrontal cortex as well, whereas others have not. The reasons for the mixed findings likely have to do with the fact that, to date, there are relatively few brain activation studies in which emotionally evocative stimuli have been presented to people with schizophrenia. Furthermore, differences in scanning methods, in emotional stimuli used and task instructions, and in participant characteristics (e.g., differences in medication, years of illness, severity of symptoms) contribute to the differences across studies. For example, studies often examine the difference between brain activation in response to an emotional stimulus (e.g., picture of puppies) compared to brain activation in response to a neutral stimulus (e.g., picture of a chair) by subtracting brain activation to the neutral stimulus from brain activation to the emotional stimulus.. However, some studies find that people with schizophrenia show greater activation to neutral stimuli compared to people without schizophrenia; thus the results of such subtractions might suggest under-recruitment of a particular brain region (e.g., the amygdala) when in fact activity in response to emotional stimuli is comparable or even greater among people with schizophrenia.Studies with healthy participants may be particularly relevant when interpreting these mixed findings. For example, studies of the perception of facial expressions find relatively more robust brain activation in areas such as the amygdala, parahippocampal cortex, pregenual cingulate, and dorsal portions of the inferior frontal gyrus. By contrast, studies that present evocative stimuli and ask participants to report on their feelings find relatively greater activation in other areas such as the prefrontal cortex (ventromedial, orbitofrontal, dorsolateral), anterior insula, medial temporal lobe, ventral inferior frontal gyrus, and temporal pole (Wager et al., 2008). Making the picture even more complicated, studies suggest that reporting on feelings is associated with activation in more dorsal/rostral areas of the medial prefrontal cortex, whereas reporting on the affective properties of a stimulus (e.g., identifying something as positive or an expression as angry) is associated with activation in more ventral portions of the medial prefrontal cortex (e.g., Ochsner, 2008). Thus, when interpreting brain activation findings in schizophrenia, it is important to consider the type of stimuli presented (e.g., faces, other evocative stimuli) and the type of task instruction (e.g., rating feelings vs. rating stimuli).Despite these complexities and differences between studies, the findings of comparable physiology and reported experience among people with and without schizophrenia despite possible differences in brain activation raises the intriguing possibility that people with schizophrenia are recruiting the brain differently to end up with the same behavioral result (i.e., comparable reports of emotional experience). The upsurge of interest in linkages among emotion, motivation, and cognition in schizophrenia alongside technological advances in imaging will promote further collaborations between affective and cognitive neuroscientists. Thus we will know a great deal more about how the brain supports emotional experience among people with schizophrenia in the very near future.Linking Emotion and CognitionOne of the paradoxes that emerged from the findings on emotional experience in schizophrenia is a discrepancy between laboratory studies and clinical ratings. Specifically, many people with schizophrenia receive a clinical rating of anhedonia, indicating that they have diminished experience of positive emotion. Yet in the presence of emotionally pleasant things, such as films, pictures, tastes, or just day-to-day life, people with schizophrenia report experiencing as much pleasure as do people without schizophrenia. Drawing upon research on the reward system in humans and animals, Kring (1999) argued for the importance of considering the temporal course of pleasure to distinguish anticipatory from in-the-moment pleasure. When people with schizophrenia are presented with pleasurable stimuli either in a lab or in daily life, they can and do derive pleasure from these experiences.However, evidence now supports the contention that people with schizophrenia appear less likely to anticipate that future events will be pleasurable, are less likely to experience pleasure in anticipation of things to come, and thus may be less likely to seek out pleasurable experiences (Gard, Kring, Germans Gard, Horan, & Green, 2007). Other behavioral and fMRI studies also find that people with schizophrenia have difficulties in what we call anticipatory pleasure. This term encompasses both the anticipation of future pleasurable experiences as well as the experience of pleasure in anticipation of future events.The ability to anticipate whether something in the future will be pleasurable requires complex cognitive skills, such as imagination, reflection, drawing upon past experiences, and maintaining an image or emotional state. Thus, the latest wave of research on emotion in schizophrenia explicitly integrates emotion and cognition, or feeling and thinking. What do we mean by cognition? Broadly, cognition refers to a set of mental or thought processes, such as attending, thinking, remembering, perceiving, and deciding. In Figure 1, we point to several emotion–cognition interactions that come into play in the temporal experience of pleasure. For example, consider the problem of what to have for dinner. You consider pizza, which may then lead you to summon a past experience of eating pizza from the neighborhood pizzeria (activating a representation and holding this in working memory), which prompts you to predict that the pizza will be very enjoyable; indeed you experience pleasure now, knowing you will soon be eating tasty pizza (i.e., anticipatory pleasure). These processes will support your motivational system such that you will order and pick up the pizza (approach motivation and behavior), and once you eat it, you will experience in-the-moment or consummatory pleasure. You will savor (maintain) the pleasure from the pizza, and this experience will be encoded into memory. Thus, the next time you contemplate dinner, this memory may be called upon to kick-start the process all over again.Fig. 1A model of the temporal experience of pleasure. A pleasurable experience may involve activating a cognitive representation of a past, related experience that will then trigger a process of predicting or anticipating what the new experience will feel like as well as a feeling of pleasure knowing that the experience is going to be happening in the future. These anticipatory processes will activate the motivation and behavior to go after or approach the experience. In the moment of “consuming” the experience, pleasure is experienced and savored or maintained so that it will be remembered at a later time.Cognitive and affective neuroscience research with healthy people has clearly demonstrated that the brain is not simply divided into regions specific to our psychological concepts, such as cognition and emotion. Instead, overlapping brain regions support thinking and feeling in interesting and complex ways (e.g., Barrett, 2009). Understanding cognition–emotion interactions is also at the forefront of research on mental illness (Taylor & Liberzon, 2007).Cognitive neuroscience findings in healthy people suggest that our ability to forecast relies on our ability to remember the past (e.g., Schacter, Addis, & Buckner, 2007), with a core network of brain regions, including areas of the medial prefrontal and medial temporal cortex, supporting both abilities. Thus, when we imagine what it will be like to have a tasty dinner with friends, we likely draw on our past experiences with dinners and friends to help imagine this future experience. Maintaining and processing emotional experiences as they occur no doubt facilitates the development of memories for these experiences, and evidence from psychophysiological and fMRI studies finds that people with schizophrenia appear to have difficulty holding on to these experiences (Horan, Wynn, Kring, Simons, & Green, 2010; Kring, Germans Gard, & Gard, 2010; Ursu et al., in press).Only a few studies to date have examined whether people with schizophrenia can retrieve memories of their emotional experiences, and even fewer have examined the relationship between memory and anticipation. One study found that people with schizophrenia were able to recall their feelings about positive films and foods 4 hours later (Horan, Green, Kring, & Neuchterlein, 2006). However, the majority of the work in this area focuses on recalling emotional stimuli (which is distinguishable from remembering feelings). For example, one study found that people with schizophrenia had difficulty recalling positive emotional stimuli 24 hours later (Herberner, Rosen, Khine, & Sweeney, 2007). Research with healthy people has found that emotionally arousing events and stimuli are remembered better than neutral ones. However, individuals with schizophrenia may not exhibit this enhancement for remembering emotional stimuli (Hall, Harris, McKirdy, Johnstone, & Lawrie, 2007).\A study that investigated the link between memory and anticipation in schizophrenia found that people with schizophrenia recalled fewer specific memories and generated fewer specific anticipated future events than did people without the disorder (D’Argembeau, Raffard, & van der Linden, 2008). It will be particularly important to explicitly examine the linkage between envisioning the future and remembering the past, particularly for emotional events among people with schizophrenia, both at the behavioral and neural levels.Other investigators have begun to examine how cognitive control, which refers to a broad array of processes including direction of attention to relevant information, maintenance of contextual information to guide behavior, and monitoring of novel information for its relevance to current goals, can influence emotional experience. For example, Dichter, Bellion, Casp, and Belger (2009) examined how, among people with and without schizophrenia, attention and emotion interact. The daily-life analog to this type of experiment might be paying attention to road signs on your way to a destination despite a screaming toddler in the backseat of your car. Findings indicated that healthy individuals activated different brain regions to facilitate attention to the demands of a task (e.g., more dorsal regions of the prefrontal cortex) while at the same time inhibiting attention to emotionally distracting information (e.g., more ventral areas of the prefrontal cortex), whereas people with schizophrenia did not. Ursu et al. (in press) found that people with and without schizophrenia exhibited comparable activations in the ventromedial prefrontal cortex while viewing emotionally evocative pictures. However, healthy controls continued to show activation in the dorsolateral and ventromedial prefrontal cortex during a 12-second delay between picture viewing and reporting emotional experience, presumably reflecting the active maintenance and control of their feelings, whereas people with schizophrenia did not show this persistent activation.Toward the next step of translation: Assessment and TreatmentThe next step of translational research on emotion and schizophrenia—that is, research translating laboratory findings to the development of new assessment and treatments—is well underway. For example, the Collaboration to Advance Negative Symptom Assessment (CANSAS) is a currently ongoing multisite study developing and validating a new clinical measure of negative symptoms (CAINS). The CAINS includes items to assess the five consensus negative symptoms: flat affect, alogia, anhedonia, asociality, and avolition. Importantly, the measure includes questions to distinguish anticipatory and in-the-moment pleasure to better assess the nature of anhedonia in schizophrenia. Once the 3-year CANSAS study is completed, the new measure will be ready for dissemination for use in treatment trials and other research pertinent to elucidating negative symptoms.Translational research over the past decade has also informed the development of psychosocial treatments that target not just symptoms but also specific emotional and cognitive difficulties. For example, cognitive behavior therapy has been successfully used as an adjunctive treatment to medications for symptoms such as disorganized thinking, delusions, and hallucinations (Wykes, Steel, Everitt, & Tarrier, 2008). More recently, it has been modified to more explicitly target the negative symptoms in schizophrenia. Preliminary data on an emotion-focused meditation treatment targeting anticipatory pleasure and motivation difficulties in schizophrenia are also promising (e.g., Johnson et al., 2009). In the next 10 years, additional efforts to develop treatments that selectively target the specific emotional difficulties in schizophrenia will likely yield much promise, thus fully realizing the potential of translational research. That is, efforts to better uncover specific deficits in schizophrenia (e.g., links between anticipation and remembering salient emotional experiences) along with the causes of these deficits (e.g., disrupted connections between brain areas supporting emotion and anticipation/memory) will allow us to develop more targeted interventions, whether pharmacological or psychosocial, for these mechanisms rather than for broad categories like negative symptoms.AcknowledgmentsWe thank Marja Germans Gard and David Gard for their contributions to the development of the model presented in Figure 1.FundingDuring preparation of this article, the author was supported by a grant from the National Institute of Mental Health (RO1MH082890-01A1).FootnotesRecommended ReadingGard, D.E., Kring, A.M., Germans Gard, M., Horan, W.P., & Green, M.F. (2007). (See References). A recent paper illustrating the deficits in anticipatory pleasure among people with schizophrenia.Kring, A.M., & Moran, E.K (2008). 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