Links between ‘empowerment’ and HIV risk
Tony Klouda - April 2008
We should not be worried about finding a definite causal link between what we call ‘empowerment’ and the
extent of protection against HIV. This is because humans are so variable, have so many different types of
factor that influence them and have so many different types of response to those factors. In any type of
intervention, different people will have different reactions and will experience different types of advantage or
disadvantage. All we have to do is to show the extent of the association by comparing the levels of
protection in different groups.
Suppose, at the end of CARE’s Strategic Impact Inquiry, we correlate all the results from the countries and
try to assess the strength of the link between empowerment (however defined) and the extent to which
people protect others and themselves in relation to HIV in their sexual interactions with others.
We will have measured increases in social efficacy (or some such measurement of empowerment) and we
will have measured extent of protection against HIV.
We will therefore have four essential measurements:
1. Numbers who have increased social efficacy who have high HIV risk
2. Numbers who have increased social efficacy who have low HIV risk
3. Numbers whose social efficacy is low who have high HIV risk
4. Numbers whose social efficacy is low who have low HIV risk
This will be put in the form of the following table to assess the possible correlation between social efficacy
and HIV risk. (The numbers are for example only. They don’t represent any real findings to date, the real
figures may be very different):
HIV risk high
HIV risk low
Social efficacy
increased
250
400
650
Social efficacy
low
320
260
580
570
660
1330
In this theoretical example the probability of HIV risk in the group whose social efficacy has remained the
same or is lower is 320/580 = 0.5517, or 55%
The probability of HIV risk in the group with increased social efficacy is 250/650 = 0.446, or 44.6%
So it looks as though the probability of getting HIV is lower in the group with higher social efficacy.
This does not mean that there is any direct or simple causal link between social efficacy and HIV risk. This is
obvious because there are so many people with what we measure as ‘low social efficacy’ who have low HIV
risk, and, similarly, there are people with what we measure as ‘increased social efficacy’ who have a high
HIV risk.
Whatever the nature of the group being studied, this is exactly the type of mix we can expect (although the
actual numbers may be very different).
In order to understand the different balances we have to probe much more deeply into the characteristics of
the different people in these four over-simplified groups. What are their social situations? What degree of
importance do they give to social cohesion? What factors allow them to be more independent of their
obligations to or dependence on social relationships (they may be richer, or come from more supportive
backgrounds, what attitudes do they have to their own bodies, what do they want to achieve with sex and
relationships, etc.)?
Many of the countries will be exploring such complexities, but because there are so many possible variables
that determine the level of risk people want to accept or take with each other, they will only be able to point
at relative strengths of association and not to causality. They will not be able to say with any confidence “this
particular intervention will reduce HIV risk by this amount”. They may, however, be able to say with a bit of
confidence, “this type of intervention has a strong association with improvement for this particular type of
person or relationship, but not for those types of person or relationship”.